Information on Anti Aging, Age Management, Bio Identical Hormone Replacement Therapy.

Jun 29 2012

FAQ on Testosterone Therapy – Women

Published by under Anti Aging - Hormones

1. What should my testosterone levels be? How do I interpret the results?
While there are no standardized, agreed upon thresholds for what is “normal” testosterone levels at this point, we do find that women who have total testosterone levels of less than 20 ng/dl and free testosterone of 0.9 or less do have symptoms of low libido and/or response.
If your testosterone is low, you can talk to your doctor about potentially replacing your testosterone. If you feel like your sexual response is low and that is feeding into your lack of interest due to pain, dryness, or lack of response or arousal, or physical release, you should consider seeking evaluation and treatment of sexual arousal disorder.

2. My doctor says I’m too young to have my levels checked. What can I tell him?
Tell your doctor that there has been evidence that even young women have low testosterone. We have found it extremely common, for instance, in pre-menopausal women after childbirth.

3. I’m taking estrogen replacement therapy. Can I have my levels checked? Does estrogen replacement affect testosterone levels?

Yes, you can have your levels checked and yes, estrogen can affect testosterone levels. When you replace estrogen without testosterone, the testosterone becomes bound to the cells, increasing something called steroid hormone binding globulin (SHBG). As less testosterone becomes available for the body to use, your levels of free testosterone decrease. You should definitely be checked, and if your testosterone levels are low think about switching to a combined replacement therapy.

No responses yet

Jun 29 2012

FAQ on Testosterone Therapy – Women

Published by under Anti Aging - Hormones

1. What should my testosterone levels be? How do I interpret the results?
While there are no standardized, agreed upon thresholds for what is “normal” testosterone levels at this point, we do find that women who have total testosterone levels of less than 20 ng/dl and free testosterone of 0.9 or less do have symptoms of low libido and/or response.
If your testosterone is low, you can talk to your doctor about potentially replacing your testosterone. If you feel like your sexual response is low and that is feeding into your lack of interest due to pain, dryness, or lack of response or arousal, or physical release, you should consider seeking evaluation and treatment of sexual arousal disorder.

2. My doctor says I’m too young to have my levels checked. What can I tell him?
Tell your doctor that there has been evidence that even young women have low testosterone. We have found it extremely common, for instance, in pre-menopausal women after childbirth.

3. I’m taking estrogen replacement therapy. Can I have my levels checked? Does estrogen replacement affect testosterone levels?

Yes, you can have your levels checked and yes, estrogen can affect testosterone levels. When you replace estrogen without testosterone, the testosterone becomes bound to the cells, increasing something called steroid hormone binding globulin (SHBG). As less testosterone becomes available for the body to use, your levels of free testosterone decrease. You should definitely be checked, and if your testosterone levels are low think about switching to a combined replacement therapy.

No responses yet

Sep 23 2010

Testosterone for Women?

Johns Hopkins Health Alert
Testosterone for Women

Comments (0)

If a woman’s sexual problems are biological rather than psychological, testosterone therapy may help.

Men may have grabbed the sexual spotlight with Viagra (sildenafil citrate) and erectile dysfunction (ED), but women are equally prone to have concerns about their sex lives. While there may not be a woman’s equivalent to Viagra, if you are concerned about sex, take comfort in knowing that you are not alone. Upwards of 43% of women report some degree of dissatisfaction with their sexual health — and help is available.

Experts believe that in women, the physical aspect of desire is governed by the male sex hormone, testosterone. Men and women produce both sex hormones, though not in equal amounts. By menopause, a woman produces 50% as much testosterone as she did in her 20s. The loss of testosterone occurs gradually over many years and is unrelated to menopause; however, its impact on desire becomes most evident around menopause, when estrogen production drops off completely. Many experts believe that boosting women’s testosterone levels will improve their libido.

The International Journal of Impotence Research recently reviewed 12 trials comparing testosterone replacement with placebo iACn postmenopausal women taking estrogen and concluded that testosterone therapy stimulates sexual desire and improves sexual satisfaction. The North American Menopause Society (NAMS) has come to similar conclusions and recommends testosterone to treat hypoactive sexual desire disorder (HSDD).

Currently, though, the only testosterone product approved by the FDA for women is Estratest, a combination of estrogen and methyltestosterone (a type of testosterone that can be taken orally). It is approved only to relieve hot flashes. Still, many doctors prescribe the treatment “off-label” — outside of its FDA-approved use — for low desire. Testosterone products approved for men also are sometimes prescribed off-label for women. Less commonly, doctors may use testosterone injections.

There are some safety concerns with long-term testosterone use. A large epidemiological study of postmenopausal women published in the Archives of Internal Medicine reported an association between an increased risk of invasive breast cancer and the use of testosterone and estrogen. NAMS recommends women use testosterone along with estrogen, as it is used in most clinical trials, but that they use it for no more than six months.

Despite these concerns, Leonard DeRogatis, Ph.D., Director of The Center For Sexual Medicine at Sheppard Pratt and a Hopkins faculty member says, “It is highly unlikely that testosterone contributes to breast cancer.” The biggest problem with transdermal (through the skin) versions of testosterone is the potential for facial hair growth and transient acne. In severe instances methyltestosterone can cause liver toxicity, but these effects can be avoided by careful monitoring. “The testosterone patch is probably the most effective delivery system; however, it is not yet available in the United States,” says Dr. DeRogatis.

Although Dr. DeRogatis believes that women will someday benefit more fully from testosterone, he says they should expect to see effective nonhormonal therapies for HSDD in the future: “Some are in the making and development is likely to be pushed along as a result of women beginning to demand more options to improve their sex life.”

Taken from the March 2007 issue of the Johns Hopkins Medical Letter: Health After 50.

No responses yet

Jun 22 2010

Adrenal Fatigue – What is adrenal fatigue

The adrenal glands, two crescent-shaped glands that sit on top of each kidney, are responsible for regulating the body’s response to stress by controlling the hormones released during stress. Adrenaline, noradrenaline, cortisol, DHEA, estrogen, progesterone and testosterone are all produced in the adrenal glands. These are the hormones that regulate energy production, immune function, heart rate, muscle tone, and other processes necessary to cope with stress. Excessive stress can impair the functioning of the adrenal glands causing a decrease in the output adrenal of hormones, especially cortisol. When this occurs, it leads to adrenal fatigue.

Adrenal fatigue has been known by many other names throughout the past century, including non-Addison’s hypoadrenia, sub-clinical hypoadrenia, neurasthenia, adrenal apathy, and adrenal exhaustion. Although it affects millions of people in the U.S. and around the world, conventional medicine does not yet recognize it as a distinct syndrome. Chronic, severe fatigue is the major complaint of patients with adrenal fatigue. However, adrenal fatigue is often associated with broad spectrum non-specific symptoms making it difficult to diagnose.

What Causes Adrenal Fatigue?

The major insult to the adrenals is caused by either a very intense single stress, or by chronic, repeated stresses that have a cumulative effect. Many times the cause of adrenal fatigue is not obvious because it can be due to a combination of factors. The stress can be physical, emotional, psychological, environmental, infectious, or a combination of these. The adrenals respond to every kind of stress the same, whatever the source. Some examples of stress that can lead to improperly functioning adrenal glands include, poor diets, lack of exercise, use of stimulants (caffeine, nicotine, amphetamines), lack of sleep, lack of relaxation, illness, overwork, major surgery, financial pressures, negative altitudes and beliefs, fears, marital stress, smoking, death of a loved one, stressful job, and recurring bouts of respiratory infections.

Signs and Symptoms
Continuing fatigue not relieved by sleep
Lethargy (lack of energy)
Feeling rundown or overwhelmed
Increased effort to perform daily tasks
Decreased ability to handle stress
Gaining weight, especially around the waist
High frequency of getting the flu and other respiratory diseases
Increased time to recover from illness, injury or trauma
Less enjoyment or happiness with life
Reduced sex drive
Lightheaded when rising from a horizontal position
Thoughts less focused, more fuzzy and memory less accurate
Afternoon low between 3 to 5 pm
Feel better suddenly for a brief period after a meal
Feel more awake, alert and energetic after 6 pm than during the day
Often feel tired from 9 – 10 pm, but resist going to bed
Need coffee or stimulants to get going in the morning
Cravings for salty, fatty, and high protein food such as meat and cheese
Increased symptoms of PMS for women
Pain in the upper back or neck with no apparent reason
Difficulties in getting up in the morning
Mild depression
Food and or inhalant allergies
Dry and thin skin
Hypoglycemia
Low body temperature
Nervousness
Palpitation
Unexplained hair loss
Alternating constipation and diarrhea
Diagnosis

None of the standard laboratory tests currently in use are designed to detect adrenal fatigue. However, there are tests that may contribute to an assessment. One such test, known as postural hypotension, occurs if blood pressure drops when a person stands up from a lying position. Postural hypotension almost always indicates low adrenal function. Another test involves checking cortisol levels either in blood, saliva or urine. Cortisol levels vary throughout the day and are highest between 6-8am. A low 8:00am plasma cortisol level can indicate poorly functioning adrenal glands. Some clinicians prefer testing cortisol levels in saliva because cortisol levels fluctuate during the day. Checking salivary cortisol can easily be done 4 or more times in a day and may detect an abnormality missed by a single blood test. The ACTH (adrenocorticotropic hormone) stimulation test can also used to diagnose poor adrenal function. ACTH is a pituitary hormone that stimulates the adrenal glands to secrete cortisol. When ACTH is injected, there should be an increase in cortisol production. If this does not happen, adrenal fatigue is probable.

Treatment

Treatment begins with an attempt to relieve stressful situations as much as possible. Initiate lifestyle changes, including diet modification and exercise. Limit the consumption of processed foods, alcohol and tobacco because these substances put extra stress on the adrenal glands. Take small breaks to lie down during the day, increase relaxation, eat regular meals, exercise regularly, get to bed early and sleep until at least 9:00 a.m. whenever possible. Try laughing because it increases parasympathetic output which reduces stress and blunts the release of excessive cortisol. Remove negative people from your life and do something fun each day

Below is a list of nutritional supplements that may also offer additional benefits to patients experiencing adrenal fatigue.

Vitamin C 2,000-4,000 mg/day
DHEA 50 mg a day
L-theanine 100-400 mg a day
Vitamin E w/mixed tocopherols 800 IU/day
Vitamin B complex
Melatonin 300 mcg-6 mg (at bedtime)
Niacin (125-150 mg/day) – as inositol hexaniacinate
B-6 150 mg/day
Phosphatidylserine capsules 300 mg a day
Pantothenic acid 1200-1500 mg/day
Magnesium citrate 400-1200 mg
Liquid trace minerals (zinc, manganese, selenium, chromium, molybdenum, copper, iodine)– calming effect

If depression is present – Add SAM.e 200 mg bid; DL-Phenylalanine (DLPA) 500 mg bid
Licorice (Glycyrrhiza glabra) no more than 1000 mg of glycyrrhizin
A diet that would be conducive to treating adrenal fatigue includes one that combines unrefined carbohydrates (whole grains) with protein and oils at most meals—olive, walnut, fiber, flax and high-quality fish oil. It is also important for patients to eat regular meals, avoid junk food and eat a diet with emphasis on vegetables. It may be of additional benefit that patients add sea salt to their diet.
Some herbal remedies that have been noted as possible therapies include Licorice, Ashwagandha, Maca, Siberian Ginseng, and Korean Ginseng. There are several glandular extracts on the market that contain adrenal, hypothalamus, pituitary, thyroid, and gonads that are also often recommended. Physiologic replacement of oral cortisone, DHEA, Pregnenolone, and Progesterone under the supervision of a physician may also be very helpful.

No responses yet

Aug 03 2009

Progesterone deficiency

Do you suffer from anxiety, depression, irritability, insomnia, muscle pain, inflammation, osteoporosis, decreased HDL-cholesterol levels, weight gain, breast tenderness, decreased libido, heavy periods, dizziness, difficulty concentrating, extreme changes in mood, bloating, and urinary incontinence? If so, you may be deficient in progesterone. Other possible symptoms of low progesterone may include frequent urinary tract infections, interstitial cystitis, changes in appetite, hot flashes, chills and night sweats. Progesterone plays a key role in the tasks necessary for reproduction. Beyond preparation for pregnancy, progesterone has a multitude of effects throughout the body, many of which help oppose the action of estrogen. Numerous physical and psychological problems can be caused by an imbalance between estrogen and progesterone including the symptoms listed above.

A number of factors can cause low progesterone levels. Including:

Stress

Antidepressants

Sugar

Saturated fat

Deficiency of vitamins A, B6, C, zinc

Decreased thyroid hormone

Impaired progesterone production

Excessive arginine consumption

Increased prolactin production

Natural or bio identical progesterone vs. synthetic Progestin

Progesterone is often confused with Progestin. Progestins are synthetic hormones made to mimic the actions of progesterone but have many negative side effects. Bio identical progesterone (also sometimes referred to as natural or human identical) is made from soy or yam and has the exact molecular structure as progesterone made in the human body. Bio identical progesterone is protective against uterine and breast cancer, balances estrogen, acts as a diuretic, builds bone, aids in sleep, restores libido, lowers cholesterol, increases scalp hair, decreases PMS symptoms, decreases carbohydrate cravings and has a natural calming effect. Progestins on the other hand have been known to cause blood clots, fluid retention, acne, weight gain, depression, an increase in heart disease and diabetes.

Griffin Medical prescribes only bio identical progesterone to patients that are deficient after a thorough physical exam and check of blood levels.

Judi Goldstone M.D.

1650 Adams Avenue

Costa Mesa, CA 92626

(714) 549-6580

No responses yet

Jul 15 2009

The Effects of Estrogen

The importance of balanced and adequate levels of estrogen is tantamount to good health in women.

What are the symptoms and causes of excessive estrogen?

Excessive estrogen, also referred to as estrogen dominance, can cause many unpleasant symptoms and lead to some very serious health issues. Over-stimulation from estrogen of the breast tissue can cause tenderness, swelling, and fibrocystic breasts. In the uterus, excess estrogen stimulation may lead to endometriosis, cervical dysplasia, increased risk of uterine cancer, heavy or irregular menses, menstrual cramping and uterine fibroid tumors. Excessive estrogen can also cause weight gain, constipation, cyclical headaches and migraines, depression, mood swings, fluid retention, low libido, and anxiety.

Women can become estrogen dominant for many reasons. Lack of exercise, impaired elimination of estrogen, not taking in enough dietary fiber, lack of adequate amounts of progesterone to balance estrogen, using birth control pills, and environmental exposure.. Estrogen mimickers are everywhere in the environment in the form of chemicals (xenoestrogens), and foods and plants (phytoestrogens). Pesticides are perhaps the biggest source of xenoestrogens followed by plastics, fuels, drugs, cosmetics, non organic meats and some dairy products. Here are some key points to reducing estrogen dominance:

• Avoid chemical sources of estrogen (xenoestrogen)
• Avoid food sources of estrogen (phytoestrogens)
• Cleanse the liver
• Reduce stress
• Balance Hormones with bio identical estrogen and progesterone
• Metabolize excess estrogen using a supplement like DIM or Breast Health Complete
• Do not heat food in plastic
• Drink out of glass containers, not plastic or Styrofoam
• Exercise

Judi Goldstone M.D.
Board Certified Internal Medicine
Specializing in Age Management Medicine and
Bioidentical Hormone Replacement Therapy
1650 Adams Avenue
Costa Mesa, CA 92626
www.griffinmedical.com
(714) 549-6580

No responses yet

Apr 10 2009

Omega-3 protect prostates from cancer

Increased intake of omega-3 fatty acids protect against advanced prostate cancer, according to new research from the University of California San Francisco.
According to findings published in the journal Clinical Cancer Research, omega-3 essential fatty acids may reduce prostate cancer risk by modifying a specific variant of the COX-2 gene, a known contributor to chronic inflammation.
The variant known as rs4647310 is linked to a five-fold increased risk of advanced prostate cancer, report the researchers, but high intakes of omega-3 may reduce the risk, even if people carry the COX-2 variant.
The highest average intakes of omega-3 fatty acids were associated with a 63 percent reduction in the risk of aggressive prostate cancer, compared to men with the lowest amount of long chain omega-3 fatty acids, said the researchers.
.

The study adds to a growing body of evidence linking omega-3 to potential cancer benefits. Results in the journal Cancer Epidemiology, Biomarkers & Prevention reported that higher intake of the omega-3 fatty acids DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid) may cut the risk of developing prostate cancer by 40 per cent. Interestingly, the new study reports no relationship between fish intake and the risk of prostate cancer.
Over half a million new cases of prostate cancer are diagnosed every year worldwide, and the cancer is the direct cause of over 200,000 deaths. More worryingly, the incidence of the disease is increasing with a rise of 1.7 per cent over 15 years.

No responses yet

Feb 04 2009

Resveratrol and 60 Minutes

Seventeen years ago, 60 Minutes first examined the so-called French paradox, which suggested that the French – despite a high fat diet and high consumption of wine – had a remarkably low incidence of heart disease, compared with Americans. Most researchers agreed that there was something in the wine that offered protection, and a few years later, even the highly cautious federal dietary guidelines say that moderate consumption of red wine can be beneficial.

Now, scientists across the country have identified a substance in red wine called resveratrol that they believe might do more than just protect the heart, but could – in very high concentrations – significantly extend life by preventing a number of age related illnesses. If they’re right, we all may soon be taking a pill that could give us an extra decade or two of healthy old age.

——————————————————————————–

“If the promise holds true, I think this has the chance to change healthcare,” Dr. Christoph Westphal tells correspondent Morley Safer.

Dr. Westphal says we all may soon be taking a drug that just might beat the clock, a simple pill that could delay the inevitable. “Our goal is to prevent and forestall many of the diseases that strike us as we reach 50, 60, and 70. All with one pill.”

Continue Reading »

No responses yet

Jan 20 2009

Turmeric Component Protects Against Toxic Compound Consumed in Many Meals

Curcumin, the pigment that gives turmeric its yellow color, may reduce the damaging effects of acrylamide (AA), a potential carcinogen created when starchy foods are baked, roasted, fried or toasted.

Swedish scientists first reported on acrylamide’s widespread presence in the food supply in 2002, when they found unexpectedly high levels of acrylamide in carbohydrate-rich foods. This was of concern since the toxin causes cancer in laboratory rats. Other scientists have found that acrylamide causes DNA to fragment, increases formation of damaging reactive oxygen species (ROS) and triggers the death of liver cells. It is also genotoxic, meaning that it damages a cell’s genetic material affecting the cell’s integrity. Genotoxic substances have the potential to be carcinogens and can cause genetic mutations that lead to the development of tumors.

Due to its antioxidant abilities, researchers studied curcumin’s effects on human liver cells exposed to acrylamide. They found that curcumin significantly reduced the production of reactive oxygen species that occurred in acrylamide-treated cells. Curcumin also inhibited the acrylamide-induced DNA fragments and significantly reduced the acrylamide-triggered cell death, indicating curcumin could ameliorate acrylamide’s known genotoxicity.

The researchers believe that curcumin’s effects are likely due to its antioxidant abilities. They concluded, “Consumption of curcumin may be a plausible way to prevent AA-mediated genotoxicity.”

Reference:

Cao J, Liu Y, Jia L, Jiang LP, Geng CY, Yao XF, Kong Y, Jiang BN, Zhong LF. Curcumin Attenuates Acrylamide-Induced Cytotoxicity and Genotoxicity in HepG2 Cells by ROS Scavenging. J Agric Food Chem. 2008 Nov 14. Published Online Ahead of Print.

No responses yet

Jan 20 2009

Grape Seed Extract May Stop Bacteria Involved in Bad Breath and Gum Disease

A new study suggests that grape seed extract may inhibit the bacteria known to cause bad breath and gum disease.

Periodontitis is a gum disease that destroys the soft tissue and bone supporting the teeth. Thirty to 50 percent of the US population suffers from the condition, which is thought to be the second most common disease worldwide.

In an in vitro study, researchers investigated whether grape seed extract could inhibit Porphyromonas gingivalis and Fusobacterium nucleatum, bacteria responsible for both periodontitis and bad breath. The researchers tested the effects of grape seed extract (97 percent polyphenols) on these two anaerobic bacteria.

The results indicated that grape seed extract exhibited antibacterial activity against the two strains. Moreover, the grape seed extract could penetrate the biofilm that surrounded the bacteria. Biofilms serve to protect bacteria against antimicrobial agents and dental plaque’s biofilm is particularly complex.

Grape seed extract also had an antioxidant activity higher than vitamins C and E, according to measures taken with the Trolox equivalent antioxidant capacity (TEAC) test. This was important to the findings of the study because gum disease originates due to the bacteria’s presence and its biofilm protection, but the disease progresses because of an excess release of reactive oxygen species that trigger the inflammatory process. Grape seed extract’s antioxidant abilities may quench the free radicals implicated in the progression of gum disease.

The researchers concluded, “These findings indicated that GSE could be used in oral hygiene for the prevention of periodontitis.”

Reference:

Furiga A, Lonvaud-Funel A, Badet C. In vitro study of antioxidant capacity and antibacterial activity on oral anaerobes of a grape seed extract. Food Chemistry. 15 April 2009;113( 4);1037-1040. Available online prior to April publication date.

No responses yet

Jan 20 2009

Low Antioxidant Levels Linked to Asymptomatic Coronary Artery Disease

Low plasma concentrations of the antioxidant vitamins A and E and the carotenoids beta carotene and lycopene are significantly associated with atherosclerosis of the carotid arteries, a new study has found.

Atherosclerosis remains clinically mute for a long time and frequently manifests itself with an acute cardiovascular event. The possibility of detecting this disease in a subclinical phase and reducing or reversing its progression is therefore an issue of relevance.

Researchers studied 220 consecutive, asymptomatic participants and examined their carotid arteries by ultrasound to determine the thickness of the arteries and whether the arteries had developed pre-atherosclerotic lesions. A medical history also was taken, a physical examination was performed and blood samples were analyzed for concentrations of antioxidant vitamins and carotenoids.

The scientists found that low concentrations of vitamin A, vitamin E, lycopene and beta carotene were significantly associated with carotid atherosclerosis as measured by increased thickness of the carotid arteries. In addition, marginally higher body mass index and low levels of high-density lipoprotein cholesterol were also associated with carotid atherosclerosis. Other factors considered in the study (total cholesterol, low-density lipoprotein cholesterol, triglycerides and C-reactive protein) were not significantly associated with carotid atherosclerosis.

According to the researchers, “Low plasma concentrations of antioxidant vitamins (vitamins A, E and beta-carotene) and lycopene were associated with early carotid atherosclerotic lesions as measured by carotid intima-media thickness (CIMT). Regular intake of foods rich in lycopene and antioxidant vitamins may slow the progression of atherosclerosis.”

Reference:

Riccioni G, Bucciarelli T, D’Orazio N, Palumbo N, di Ilio E, Corradi F, Pennelli A, Bazzano LA. Plasma Antioxidants and Asymptomatic Carotid Atherosclerotic Disease. Ann Nutr Metab. 2008 Oct 21;53(2):86-90.

No responses yet

Jan 20 2009

The Latest Research on Fatigue, Heart Health, Cognitive Function and More

Omega-3s Linked to Prostate Health

Men who increase their intake of omega-3-rich fish have a greater chance of surviving prostate cancer, according to a new study.

Researchers studied 20,167 men who were participating in the Physician’s Health Study. The subjects were free of cancer in 1983, when the study began. During follow-up, 2,161 men were diagnosed with prostate cancer and 230 died of the disease.

Although intake of omega-3-rich fish was unrelated to prostate cancer incidence, it was linked to survival from the disease. Among the men diagnosed with prostate cancer, those consuming fish five or more times per week had a 48 percent lower risk of prostate cancer death than did men consuming fish less than once weekly.

In this study the scientists found no link between fish consumption and a reduced incidence of prostate cancer, but the same researchers conducted an earlier study that found higher intake of the omega-3 fatty acids DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid) may reduce the risk of developing prostate cancer by 41 percent.

Reference:

Chavarro JE, Stampfer MJ, Hall MN, Sesso HD, Ma J. A 22-y prospective study of fish intake in relation to prostate cancer incidence and mortality. Am J Clin Nutr. 2008 Nov;88(5):1297-303.

No responses yet

Oct 23 2008

Confusion Over Hormone Replacement Therapy – By Judi Goldstone

Published by under Anti Aging - Hormones

Women are confused, and can you blame them? Ever since the Women’s Health Initiative (WHI), hormonal replacement therapy (HRT) has become an extremely controversial topic, especially since a lot of physicians themselves have a problem explaining the results.

Dr. Judi Goldstone at Griffin Medical Group recently sat down and answered questions on the subject of bio-identical hormone replacement for women. Dr. Goldstone is an expert on the subject and these are comments to questions that were submitted to her blog.

Dr. Goldstone is a board certified internal medicine specialist and Director of the Age Management program at Griffin Medical Group. Dr. Goldstone is also an active member of the American Society of Anti-Aging Medicine (A4M).


Question
: What is the theory behind bio-identical hormone replacement therapy (HRT) in menopausal women?

Dr. Goldstone: When it comes to disease, conventional medicine will restore of low levels of thyroid, insulin and cortisol. This would be the standard and typical medical treatment. Thus, it seems logical to also replace estrogen, progesterone, testosterone growth hormone when a person has low levels of those hormones. However, the evidence leaves clinicians at a loss for clear direction, because different studies, using a variety of types of hormones, methods of hormone administration, and women of different ages, have produced conflicting results.

Question: What are the Normal Hormone Ratios?

Dr. Goldstone: There are three predominant estrogens in non-pregnant, pre-menopausal women: estrone (E1), estradiol (E2) and estriol (E3). These naturally occur in different relative amounts. Typically, E1 will make up 10 to 20 percent of total estrogen, E2 will make up another 10 to 20 percent and E3 will comprise the remaining 60 to 80 percent of total estrogen.

This ratio is protective, because the bulk of estrogen is comprised by the weakest estrogen, E3, which is also the most protective against blood clots and breast cancer. E2 is the strongest estrogen, and E1 is the storage form of estrogen. E1 is sometimes considered the “least desirable” estrogen, because it can stimulate breast tissue production and blood clots. E1 can be metabolized and excreted by the liver, but if the liver systems are overwhelmed or if vitamins B12 and folic acid are deficient, E1 is converted to quinines. These can be mutagenic and carcinogenic, and thus could ultimately lead to cancer and other health problems.

Question: What are bio-identical hormones and how can they mimic protective ratios?

Dr. Goldstone: Estrogen-like hormones can be obtained from horses, soy and yams, but these hormones do not fit exactly into the human receptors. By contrast, bio-identical hormones are an exact match, molecule for molecule, to the hormones produced naturally by a woman’s body. They fit the hormone receptor just like a key fits into its lock, and the body cannot distinguish between a bio-identical hormone and the hormones it makes itself.

Bio-identical hormones can be made in several ways. Sometimes they are created by modifying soy or yam — any molecule that does not exist on the human hormone counterpart is removed. They are produced synthetically in the laboratory to make bio-identical estrogen, testosterone and progesterone transdermal creams and gels.

Question: How are bio-identical hormones prescribed by doctors who use them today?

Dr. Goldstone: The goal is to re-establish the normal protective ratio, a 20:80 ratio of E2 to E3, and avoid E1 altogether. This formula is called Bi-est. Estrogen that comes in the form of a transdermal cream mimics normal ratios better than estrogen that is taken in pill form, because the estrogen pill first has to pass through the liver, where 50 percent is converted into E1 (“bad” estrogen) before being circulated to tissues.

Estrogen applied through a transdermal cream enters the blood at the same ratio in which it is applied to the skin, with no chance for alteration by the liver. Many studies suggest that estrogen administered through a transdermal cream decreases thrombosis, blood pressure, triglycerides and vascular resistance, as opposed to the pill form of estrogen, which is known to increase these effects and can also cause other problems.

Question: Hormone replacement studies have raised questions about the health risks associated with traditional menopause treatment, what has happened since then?

Dr. Goldstone: The Women’s Health Initiative (WHI) was a large study, sponsored by the National Institute of Health, which greatly influenced how American doctors prescribe hormones and how American women receive them. Millions of women stopped hormone replacement therapy (HRT) because of the study’s findings.

But, as with any medical study, there were many problems. The researchers did not take “quality of life” into account. They did not use estrogens in favorable ratios and they did not test hormones that were administered via a transdermal cream. The estrogen used by women in the study was a synthetic, non bio-identical and oral conjugated estrogen from a pregnant mare’s urine called Premarin, which is known to increase the risk of thrombosis and cancer. The study also used the oral estrogen mentioned above combined with progestin, which is a synthetic and non bio-identical progesterone and this to can increase the risk cardiovascular disease and cancer.

Another problem with the study was the age of the women involved. The researchers should have started women on hormone therapy before they developed significant vascular disease, by age 55, instead of at an average age of 63 and higher.

Finally, the researchers should have insisted on media coverage of some of the positive findings they later discovered in their data analysis. Since that study, many American women and their doctors have found an alternative treatment via the bio-identical hormone approach.

Unfortunately, there are no studies on bio-identical hormones comparable to the size of the WHI study available yet. While there is no question that more studies on bio-identical hormone therapies are needed, a large body of evidence points to the potential advantages of the bio-identical approach.

Yours in health,

Griffin Medical Group

www.griffinmedical.com

No responses yet

Sep 05 2008

Hypothyroidism – by Judi Goldstone, M.D.

Hypothyroidism

Hypothyroidism is a disease state whereby the thyroid gland fails to produce enough thyroid hormone. Epidemiology

In the United States studies have shown the prevalence of hypothyroidism to be anywhere from 3-10%. Internationally the prevalence has been reported as 2-5%, increasing to 15% by age 75 years. Cretinism refers to congenital hypothyroidism, which has been estimated to affect one per 4000 newborns. However, the numbers could be higher due to many cases that go undetected. Even when lab tests are in the “normal range” one must remember normal for one person may be inadequate for someone else. In my practice I look at each patient as an individual and optimize their thyroid function based on symptoms, clinical exam and lab findings. Hypothyroidism is one of the most under diagnosed hormonal imbalances of aging. It is more common in women than men and the incidence increases with age. Other risk factors include having a family history of thyroid problems, a history of chronic fatigue syndrome, female gender, age greater than 50 yrs, exposure to radiation, chemical exposure (flouride, perchlorate), obesity or a history of thyroid surgery.

Thyroid structure and function

Continue Reading »

No responses yet

Jun 27 2008

DHEA – A Naturally Safe and Effective Pro-Hormone

“A number of biological indices confi rmed the lack of harmful consequences of this 50 mg/day DHEA administration over one year, also indicating that this kind of replacement therapy normalized some effects of aging, but does not create “supermen/women” (doping).”

Proceedings of the National Academy of Science USA, 2000; 97:4279-84

Dehydroepiandrosterone (DHEA) is a naturally occurring pro-hormone produced primarily by the adrenal glands, testes in men or ovaries in women, while small amounts are also created in the liver and brain. It is known as a “precursor hormone” since it is produced in large amounts in the body and serves as the progenitor for other hormones to be produced such as estrogen and testosterone. Within both the male and female body, DHEA increases dramatically before puberty in children, usually peaks when we’re in our mid-20s, and drops off from this peak throughout the aging process. By the 40th birthday most people have a mere 50 percent of their former youthful levels. It is currently believed that this dramatic and persistent drop in DHEA is related to the aging process, including loss of muscle mass, weight gain, decreased zeal for life, diminished mental clarity, decreased bone density and countless other signs of aging.

Overview

One can succinctly summarize the role of DHEA in the human body as essential for maintaining quality of life and optimal performance. With the dramatic and persistent drop of DHEA levels during the aging process, there is no question that the ability to augment levels is essential and a liberty that should be enjoyed by all those that need to buffer age-related decreased levels or who suffer from health conditions that have been demonstrated to benefit from supplementation.

The clinical research on the use of DHEA is significant and the safety window is broad when used at reasonable and appropriate doses. As the following research summary stated: “Administration of low doses (25 mg) of DHEA positively modulates several endocrine parameters in early and late postmenopausal women, inducing the increase of the androgenic, estrogenic, and progestogenic milieu and reducing the climacteric symptoms, similarly to estroprogestin replacement therapy.”1 Thus, the conclusion is that DHEA can be as effective as hormone replacement therapy at a fraction of the cost to the American Healthcare System.

Basic Biochemistry of DHEA

DHEA and its sulfate ester, dehydroepiandrosterone sulfate (DHEA-S), are interconvertible. The importance of DHEA to human performance is well illustrated by the fact that DHEA is converted to DHEA-S, which serves as a storage form of DHEA.2-3 It is the storage of this dynamic “precursor” pro-hormone that emphasizes its critical biochemical function. When needed, DHEA-S is then converted by the body’s tissues and target organs back to DHEA. It is at the cellular level that DHEA is then converted as needed to other hormones.4

At normal, healthy levels, the concentration of DHEA-S is 100 to 500 times higher than testosterone and 1,000 to 10,000 times higher than estradiol, the body’s most potent estrogen. It is essential to realize that though DHEA serves as a precursor to sex steroid

Circulatory disease is the number one cause of death in the United States and there is now evidence that DHEA can help support the health of the 18,000 miles of the microvascular system within the body.

hormones, it does not perform a direct estrogenic or androgenic role.5 Both DHEA and DHEA-S levels are higher in men than in women and they peak at about 20 years of age and decline rapidly after age 25.6 There is a direct correlation with increased mortality and very low levels of DHEA-S in men under the age of 70. Furthermore, men who smoke and have low DHEA-S levels seem to have a mortality risk more than 6 times greater than nonsmokers with high DHEA-S levels.7

The risk of the body accumulating high levels of DHEA with supplementation of 50 mg of DHEA or less is modest at best. The highly esteemed scientific journal

Proceedings of the National Academy of Science in 2000 reported:

“Two hundred and eighty healthy individuals (women and men 60-79 years old) were given DHEA, 50 mg, or placebo, orally, daily for a year in a double-blind, placebo-controlled study. No potentially harmful accumulation of DHEA-S and active steroids was recorded. Besides the reestablishment of a ‘young’ concentration of DHEA-S, a small increase of testosterone and estradiol was noted, particularly in women, and may be involved in the significantly demonstrated physiological-clinical manifestations here reported. Bone turnover improved selectively in women over 70 years old, as assessed by the dual-energy x-ray absorptiometry (DEXA) technique and the decrease of osteoclastic activity. A significant increase in most libido parameters was also found in these older women. Improvement of the skin status was observed, particularly in women, in terms of hydration, epidermal thickness, sebum production, and pigmentation.

A number of biological indices confirmed the lack of harmful consequences of this 50 mg/day DHEA administration over one year, also indicating that this kind of replacement therapy normalized some effects of aging, but does not create “supermen/women” (doping).”49

Consequences of Lower DHEA Levels

There are several health conditions that seem more prevalent in individuals with lower DHEA levels. The conditions frequently associated with lower levels of DHEA include; but

ted to.8, 9, 10

are not limi

* Anorexia nervosa

* Chronic fatigue

* Congestive heart failure

* Depression

* Diabetes mellitus Type 2

* Erectile dysfunction

* Kidney disease (End-Stage)

* Schizophrenia

* Systemic lupus erythematosus (SLE)

Circulatory disease is the number one cause of death in the United States and there is now evidence that DHEA can help support the health of the 18,000 miles of the microvascular system within the body. The mechanism for this protective effect appears to arise from the inhibition of thromboxane A2 synthesis in platelets; this decrease in thromboxane A2 is accompanied by increased levels of insulin-like growth factor 1 (IGF-1), cyclic guanosine monophosphate (GMP) and nitric oxide synthesis.11 The ability of DHEA to naturally optimize this essential biochemical pathway and the fact that there is a significant drop in DHEA during aging, may account for the increased frequency of heart disease and the associated escalating economic costs of heart disease during the aging process.

Safe and Natural

Dehydroepiandrosterone when used orally and appropriately in the short-term has been shown in numerous studies to be safe and effective for many months.12, 13, 14, 15, 16, 17

Additional studies have used oral DHEA for 12-24 months.18, 19, 20 Another study, lasting twelve months, investigated intravaginally DHEA use with reported safety in postmenopausal women.21 DHEA is well absorbed orally and possesses a serum half-life of 15 to 38 minutes; whereas the half-life of DHEA-S is longer, at 7-22 hours. The kidneys are the primary route of elimination and account for the clearance of 51 percent to 73 percent of DHEA-S and its metabolic endproducts.12

DHEA Clinical Research Applications

There are over two dozen therapeutic applications for DHEA supplementation. The following are some of the areas that have been studied by researchers and reported in the peer-reviewed medical literature.

Adrenal Insuffi ciency

Taking low-dose DHEA orally (20-50 mg daily) has been associated with increased sense of well-being, healthier skin and hair and enhanced sexuality in women with low

23

pituitary function.22,

Addison’s Disease

Preliminary clinical evidence suggests that oral DHEA might improve symptoms of Addison’s disease.24

Aging Skin

Oral DHEA supplementation has been shown to increase epidermal skin thickness, skin hydration, and lessen facial skin discoloration in aging women and men.25

Congestive Heart Failure

Clinical researchers have reported, in a study conducted in the year 2000, that: “These results indicate that the plasma levels of DHEA-S are decreased in patients with CHF in proportion to its severity and that oxidative stress is associated with decreased levels of DHEA-S in patients with CHF.”26

Depression

Clinical use of DHEA to help lessen symptoms of depression and dysthymia (chronic depression) appear promising as reflected in a 1999 study report that states: “These results suggest that DHEA treatment may have significant antidepressant effects in

on.”27, 28

some patients with major depressi

Erectile Dysfunction (ED)

When oral DHEA is taken for 24 weeks, ED symptoms improve along with orgasmic function, libido, and overall satisfaction. Men suffering from ED secondary to high blood pressure or idiopathic causes were those that responded significantly to DHEA treatment.29, 30

Menopausal Symptoms

A 2003 report concluded, “Administration of low doses (25 mg) of DHEA positively modulates several endocrine parameters in early and late postmenopausal women, inducing the increase of the androgenic, estrogenic, and progestogenic milieu and reducing the climacteric symptoms, similarly to estroprogestin replacement therapy.”31

Metabolic Syndrome

Oral use of DHEA, 50 mg daily for 6 months, lead to significant weight reduction, less abdominal fat and improved insulin levels. The Journal of the American Medical Association published a report in 2004 that made the following conclusion, “DHEA replacement could play a role in prevention and treatment of the metabolic syndrome associated with abdominal obesity.”32 With approximately 50 million Americans suffering from Metabolic Syndrome according to the Centers for Disease Control (CDC), this application for DHEA could help lessen the current conversion rate to diabetes that is at a staggering 1.5 million new cases per year.

Osteoporosis

Older men and women with osteoporosis or osteopenia have benefited from an oral dose of DHEA at 50-100 mg daily. These study participants experienced increased bone density.33, 34 Likewise, young women with osteoporosis secondary to anorexia nervosa can often benefit.35

Systemic Lupus Erythematosus (SLE)

Compelling evidence suggests that DHEA administered orally in conjunction with standard medical treatment, can help lessen SLE disease activity, frequency of flare-ups, and the number of glucocorticosteroid doses

38, 39, 40, 41

needed.36, 37,

Vaginal atrophy

Vaginally, application of DHEA appears to be effective for the treatment of vaginal atrophy in postmenopausal women and may also confer a secondary benefit of increased bone mineral density.42

Common Clinical Dosing in Research Studies

Please note that none of the research presented in this paper is intended to serve as either treatment or diagnosis, but rather a clear demonstration of the safety and efficacy of appropriately used DHEA. In that spirit, the information that follows is simply a reflection of some representative dosages of DHEA used in clinical trials around the world. It should be noted that in order to conduct a human study, approval by an IRB (Institutional Review Board) is essential to ensure safety. Thus, the IRB process designed to protect participants in research studies must have deemed these dosages to be safe and reasonable.

In postmenopausal women, doses of 25-50 mg daily are commonly used with benefits of lessened menopausal symptoms, improved tissue insulin sensitivity and lower

44, 45, 46

serum triglycerides readings.43,

In cases of depression, doses of DHEA between 30-90 mg daily have been used, either as a stand alone intervention or in conjunction with standard antidepressant therapy. A double blind clinical trial published in 1999 reported, “These results suggest that DHEA treatment may have significant antidepressant effects in some patients with major depression.”47 An earlier 1997 study reported

It is essential to realize that though DHEA serves as a precursor to sex steroid hormones, it does not perform a direct estrogenic or androgenic role.

The Journal of the American Medical Association

published a report in 2004 that made the following conclusion, “DHEA replacement could play a role in prevention and treatment of the metabolic syndrome associated with abdominal obesity.”32

clinical benefits plus improved memory: “These preliminary data suggest DHEA may have antidepressant and promemory effects, and should encourage double-blind trials in depressed patients.”48

A schizophrenia study used increasing doses of DHEA of 25 mg daily for 2 weeks, 25 mg two times daily for 2 weeks, and 50 mg two times daily for 2 weeks. This significant 2003 report of DHEA use and schizophrenia states, “Our preliminary observations report for the first time in double-blind fashion, the efficacy of DHEA augmentation in the management of negative, depressive, and anxiety symptoms of schizophrenia. The findings from this study raise important issues regarding the role of neurosteroids in general, and DHEA in particular, in the ongoing symptomatology and pharmacotherapy of schizophrenia.”16 Dosing for systemic lupus erythematosus (SLE), can be upwards of 200 mg daily, used as addition to standard SLE medical treatment protocols.27

Bone mineral density studies investigating treatment for osteopenia or osteoporosis often use DHEA levels in the range of 50-100 mg per day.33

An erectile dysfunction study utilizing 50 mg of DHEA daily has been conducted. The researchers’ conclusion was simple, “Our results suggest that oral DHEA treatment may be of benefit in the treatment of ED.”18

In the case of prediabetes, also known as metabolic syndrome, 50 mg taken orally at bedtime was employed.33 The result of this study showed that DHEA replacement could play a role in prevention and treatment of the metabolic syndrome associated with abdominal obesity.

Conclusion

The review of the peer-reviewed medical literature clearly demonstrates not only the safety of appropriately used dosages of DHEA, it also elucidates that DHEA can help tens of millions of people alleviate the symptoms produced by drops in DHEA associated with aging and help mitigate various health conditions by optimizing DHEA levels. Clear and convincing evidence is in the medical literature; in addition, IRB boards from around the world have approved the use of DHEA in human clinical trials with a solid record of both safe and effective use. As discussed earlier in this report and stated so aptly in the findings of one of the world’s most revered medical journals, DHEA is not a “doping substance.” Scientific research has documented that DHEA helps normalize the aging process, a beneficial liberty that all humanity must be able to freely partake. Therefore, in conclusion, I will once again quote the above study that demonstrates DHEA’s safety:

A number of biological indices confirmed the lack of harmful consequences of this 50 mg/day DHEA administration over one year, also indicating that this kind of replacement therapy normalized some effects of aging, but does not create “supermen/women” (doping).”49

References

1 Genazzani AD, Stomati M, Bernardi F, et al. Long-term low-dose dehydroepiandrosterone oral supplementation in early and late postmenopausal women modulates endocrine parameters and synthesis of neuroactive steroids. Fertil Steril 2003;80:1495-501. 2 Moffat SD, Zonderman AB, Harman M, et al. The relationship between longitudinal declines in dehydroepiandrosterone sulfate concentrations and cognitive performance in older men. Arch Int Med 2000;160:2193-8. 3 Pepping J. DHEA: dehydroepiandrosterone. Am J Health Syst Pharm 2000;57:2048-50, 2053-4, 2056. 4 Oelkers W. Dehydroepiandosterone for adrenal insufficiency (editorial). N Engl J Med 1999;341:1073-4. 5 Tchernof A, Labrie F. Dehydroepiandrosterone, obesity and cardiovascular disease risk: a review of human studies. Eur J Endocrinol 2004;151:1-14. 6 Villareal DT, Holloszy JO. Effect of DHEA on abdominal fat and insulin action in elderly women and men. JAMA 2004;292:2243-8. 7 Mazat L, Lafont S, Berr C, et al. Prospective measurements of dehydroepiandrosterone sulfate in a cohort of elderly subjects: relationship to gender, subjective health, smoking habits, and 10-year mortality. Proc Natl Acad Sci U S A 2001;98:8145-50. 8 Kroboth PD, Salek FS, Pittenger AL, et al. DHEA and DHEA-S: A review. J Clin Pharmacol 1999;39:327-48. 9 Kuratsune H, Yamaguti K, Sawada M, et al. Dehydroepiandrosterone sulfate deficiency in chronic fatigue syndrome. Int J Mol Med 1998;1:143-6. 10 Reiter WJ, Pycha A, Schatzl G, et al. Serum dehydroepiandrosterone sulfate concentrations in men with erectile dysfunction. Urology 2000;55:755-8. 11 Pepping J. DHEA: dehydroepiandrosterone. Am J Health Syst Pharm 2000;57:2048-50, 2053-4, 2056. 12 Arlt W, Callies F, van Vlijmen JC, et al. Dehydroepiandosterone replacement in women with adrenal insufficiency. N Engl J Med 1999;341:1013-20. 13 Casson PR, Andersen RN, Herrod HG, et al. Oral dehyroepiandosterone in physiologic doses modulates immune function in postmenopausal women. Am J Obstet Gynecol 1995;1536-9. 14 Wit JM, Langenhorst VJ, Jansen M, et al. Dehydroepiandrosterone sulfate treatment for atrichia pubis. Horm Res 2001;56:134-9. 15 Strous RD, Maayan R, Lapidus R, et al. Dehydroepiandrosterone augmentation in the management of negative, depressive, and anxiety symptoms in schizophrenia. Arch Gen Psychiatry 2003;60:133-41. 16 Stomati M, Monteleone P, Casarosa E, et al. Six-month oral dehydroepiandrosterone supplementation in early and late postmenopause. Gynecol Endocrinol 2000;14:342-63. 17 Piketty C, Jayle D, Leplege A, et al. Double-blind placebo-controlled trial of oral dehydroepiandrosterone in patients with advanced HIV disease. Clin Endocrinol (Oxf) 2001;55:325-30. 18 Van Vollenhoven RF, Morabito LM, Engleman EG, et al. Treatment of systemic lupus erythematosus with dehydroepiandrosterone: 50 patients treated up to 12 months. J Rheumatol 1998;25:285-9. 19 Baulieu EE, Thomas G, Legrain S, et al. Dehydroepiandrosterone (DHEA), DHEA sulfate, and aging. Contribution of the DHEAge study to a sociobiomedical issue. Proc Natl Acad Sci U S A 2000;97:4279-84. 20 Genazzani AD, Stomati M, Bernardi F, et al. Long-term low-dose dehydroepiandrosterone oral supplementation in early and late postmenopausal women modulates endocrine parameters and synthesis of neuroactive steroids. Fertil Steril 2003;80:1495-501. 21 Labrie F, Diamond P, Cusan L, et al. Effect of 12 month dehydroepiandrosterone replacement therapy on bone, vagina, and endometrium in postmenopausal women. J Clin Endocrinol Metab 1997;82:3498-505. 22 Arlt W, Callies F, van Vlijmen JC, et al. Dehydroepiandosterone replacement in women with adrenal insufficiency. N Engl J Med 1999;341:1013-20. 23 Johannsson G, Burman P, Wiren L, et al. Low dose dehydroepiandrosterone affects behavior in hypopituitary androgen-deficient women: a placebo-controlled trial. J Clin Endocrinol Metab 2002;87:2046-52. 24 Kim SS, Brody KH. Dehydroepiandrosterone replacement in Addison’s disease. Eur J Obstet Gynecol Reprod Biol 2001;97:96-7. 25 Baulieu EE, Thomas G, Legrain S, et al. Dehydroepiandrosterone (DHEA), DHEA sulfate, and aging. Contribution of the DHEAge study to a sociobiomedical issue. Proc Natl Acad Sci U S A 2000;97:4279-84. 26 Moriyama Y, Yasue H, Yoshimura M, et al. The plasma levels of dehydroepiandrosterone sulfate are decreased in patients with chronic heart failure in proportion to the severity. J Clin Endocrinol Metab 2000;85:1834-40. 27 Wolkowitz OM, Reus VI, Keebler A, et al. Double-blind treatment of major depression with dehydroepiandosterone. Am J Psychiatry 1999;156:646-9. 28 Bloch M, Schmidt PJ, Danaceau MA, et al. Dehydroepiandrosterone treatment of midlife dysthymia. Biol Psychiatry 1999;45:1533-41. 29 Reiter WJ, Pycha A, Schatzl G, et al. Dehydroepiandosterone in the treatment of erectile dysfunction: A prospective, double-blind, randomized, placebo-controlled study. Urol 1999;53:590-5. 30 Reiter WJ, Schatzl G, Mark I, et al. Dehydroepiandrosterone in the treatment of erectile dysfunction in patients with different organic etiologies. Urol Res 2001;29:278-81. 31 Genazzani AD, Stomati M, Bernardi F, et al. Long-term low-dose dehydroepiandrosterone oral supplementation in early and late postmenopausal women modulates endocrine parameters and synthesis of neuroactive steroids. Fertil Steril 2003;80:1495-501. 32 Villareal DT, Holloszy JO. Effect of DHEA on abdominal fat and insulin action in elderly women and men. JAMA 2004;292:2243-8. 33 Sun Y, Mao M, Sun L, et al. Treatment of osteoporosis in men using dehydroepiandrosterone sulfate.Chin Med J (Engl) 2002;115:402-4. 34 Villareal DT, Holloszy JO, Kohrt WM. Effects of DHEA replacement on bone mineral density and body composition in elderly women and men. Clin Endocrinol (Oxf) 2000;53:561-8. 35 Gordon CM, Grace E, Emans SJ, et al. Effects of oral dehydroepiandrosterone on bone density in young women with anorexia nervosa: a randomized trial. J Clin Endocrinol Metab 2002;87:4935-41. 36 Van Vollenhoven RF, Morabito LM, Engleman EG, et al. Treatment of systemic lupus erythematosus with dehydroepiandrosterone: 50 patients treated up to 12 months. J Rheumatol 1998;25:285-9. 37 Van Vollenhoven RF, Engleman EG, McGurie JL. Dehydroepiandrosterone in Systemic Lupus Erythematosus. Arth Rheum 1995;38:1826-31. 38 van Vollenhoven RF, Engleman EG, McGuire JL. Dehydroepiandrosterone in systemic lupus erythematosus. Arthritis Rheum 1994;37:1305-10. 39 van Vollenhoven RF, Park JL, Genovese MC, et al. A double-blind, placebo-controlled, clinical trial of dehydroepiandrosterone in severe lupus erythematosus. Lupus 1999;8:181-7. 40 Petri MA, Mease PJ, Merrill JT, et al. Effects of prasterone on disease activity and symptoms in women with active systemic lupus erythematosus. Arthritis Rheum 2004;50:2858-68. 41 Petri MA, Lahita RG, Van Vollenhoven RF, et al. Effects of prasterone on corticosteroid requirements of women with systemic lupus erythematosus: a double-blind, randomized, placebo-controlled trial. Arthritis Rheum 2002;46:1820-9. 42 Labrie F, Diamond P, Cusan L, et al. Effect of 12 month dehydroepiandrosterone replacement therapy on bone, vagina, and endometrium in postmenopausal women. J Clin Endocrinol Metab 1997;82:3498-505. 43 Casson PR, Faquin LC, Stentz FB. Replacement of dehydroepiandrosterone enhances T-lymphocyte insulin binding in postmenopausal women. (abstract) Fertil Steril 1995;63:1027-31. 44 Morales AJ, Haubrich RH, Hwang JY, et al. The effect of six months treatment with 100 mg daily dose of dehydroepiandrosterone (DHEA) on circulating sex steroids, body composition and muscle strength in age-advanced men and women. [Abstract] Clin Endocrinol (Oxf)1998;49:421-32.

45 Casson PR, Andersen RN, Herrod HG, et al. Oral dehyroepiandosterone in physiologic doses modulates immune function in postmenopausal women. Am J Obstet Gynecol 1995;1536-9. 46 Barnhart KT, Freeman E, Grisso JA, et al. The effect of dehydroepiandrosterone supplementation to symptomatic perimenopausal women on serum endocrine profiles, lipid parameters, and health-related quality of life. J Clin Endocrinol Metab 1999;84:3896-902. 47 Wolkowitz OM, Reus VI, Keebler A, et al. Double-blind treatment of major depression with dehydroepiandosterone. Am J Psychiatry 1999;156:646-9. 48 Wolkowitz OM, Reus VI, Manfredi F, et al. Dehydroepiandrosterone (DHEA) treatment of depression. [Abstract] Biol Psychiatry 1997;41:311-8. 49 Baulieu EE, Thomas G, Legrain S, et al. Dehydroepiandrosterone (DHEA), DHEA sulfate, and aging. Contribution of the DHEAge study to a sociobiomedical issue. Proc Natl Acad Sci U S A 2000;97:4279-84.

As discussed earlier in this report and stated so aptly in the fi ndings of one of the world’s most revered medical journals, DHEA is not a “doping substance.”

No responses yet

Jun 16 2008

Homocysteine and Osteoporosis

Published by under Osteoporosis

Homocysteine
Its Destructive Role in Cardiovascular, Cognitive and Bone Health
By Jason E. Barker, ND

Homocysteine is one of the most destructive compounds found in the human body. Although oxidized LDL cholesterol (the “bad” cholesterol) is commonly considered the arteries’ worst enemy, homocysteine has emerged as an equally powerful threat to heart health. In fact, research now shows that damage from homocysteine paves the way for LDL to have an even more destructive effect on the vascular system, indicating these two agents can work together to cause heart disease. Furthermore, as time goes on, more and more research is uncovering homocysteine’s role in other health conditions such as infertility, depression, cognitive decline and bone fractures.

Homocysteine is considered a primary risk factor for cardiovascular disease including stroke and deep vein thrombosis.1 Elevated blood levels of homocysteine also are considered an independent risk factor for atherosclerosis and thromboembolism (the obstruction of a blood vessel by a clot), and are correlated with a significant risk for coronary, cerebral and peripheral vascular disease, myocardial infarction (heart attacks), peripheral vascular occlusive disease, cerebral vascular occlusive disease, and retinal vascular disease.2 In fact, high homocysteine, even in the absence of other risks, such as smoking and obesity, is a serious but controllable risk factor for heart disease.

Homocysteine is an amino acid commonly found in the blood as a result of protein metabolism. It is mainly derived from another amino acid known as methionine, which is found in a number of food sources primary among them being meat. Blood levels of homocysteine can also be affected by genetic and physiologic factors.

Homocysteine is thought to cause vascular disease because of its effect on blood vessel walls. Homocysteine binds to certain proteins in the body affecting their structure and function. The binding of homocysteine to proteins will degrade and inhibit repair and maintenance of three main vascular connective tissue structures—cartilage, elastin and proteolgycans—making them more susceptible to disease processes, including vascular disease. Homocysteine can damage the cells lining the artery walls (known as the endothelium) in the vascular system. Homocysteine causes a reduction in nitric oxide activity, impairing blood vessels’ ability to dilate and leaving the endothelium more susceptible to oxidative damage.3 Damaged vascular walls will then allow more low density lipoprotein (LDL) to be absorbed, further harming the vessel. This damage then promotes the growth of new smooth muscle cells within the vessel, which then narrows it. Endothelial damage also allows for increased platelet adhesiveness and activation of the clotting cascade, increasing the risk of cardiac arrest (heart attack) or cerebrovascular accident (stroke).

homocysteine Homocysteine and OsteoporosisIn the Western world, homocysteine serum levels are most commonly found at 10-12 μmol/L. A level above 12 is generally considered elevated while levels below 6 are considered minimal. An increase of homocysteine levels by 5 μmol/L has been shown to increase the risk of cerebrovascular disease in the general population by 50 percent, and will increase the risk of coronary artery disease by 80 percent in women and 60 percent in men. In general, women have 10-15 percent less homocysteine than men during their reproductive years, which is thought in part to be the reason why women have fewer heart attacks than men, and why they tend to have them 10-15 years later than the time men commonly do.4

Genetic Causes of High Homocysteine

Dietary factors, while often cited as the chief cause for elevated homocysteine, are not the only factor. A rare hereditary disease known as homocystinuria results in several systemic disorders and is charachterized by the accumulation of homocysteine in the blood and an increased rate of excretion in the urine. Nearly 25 percent of people with this disorder die from cardiovascular complications before the age of thirty.

Ten percent of the population in general have another more common yet related condition where they are unable to effectively metabolize homocysteine and will be predisposed to the negative effects of elevated homocysteine levels, including blood clots and cardiovascular disease. This disorder is known as a methylenetetrahydrofolate-reductase (MTHFR) polymorphism genetic trait. People that have this condition are unable to effectively metabolize homocysteine and will be predisposed to the negative effects of elevated homocysteine levels, including blood clots and cardiovascular disease.

Homocysteine’s Widespread Role

Elevated homocysteine, also known as hyperhomocysteinemia, may contribute to many other conditions.

Infertility

Women who have high levels of homocysteine have been shown to have a more difficult time getting pregnant and are two times as likely to have complications during pregnancy. Furthermore, women with high homocysteine levels are at risk of having miscarriages early in pregnancy.5-6 Researchers are not sure what role homocysteine has in infertility, but it has been theorized that high homocysteine contributes to subfertility, or difficulty achieving a pregnancy.

Mental Health

Elevated levels of homocysteine are also a risk factor for diseases affecting the brain. Epidemiologic studies show a dose-dependent relationship between homocysteine levels and risk for neurodegenerative diseases such as stroke, Parkinson’s disease, multiple sclerosis, and depression.7 Researchers continue to collect evidence that correlates several cardiovascular disease risk factors, homocysteine being one, with the incidence of cognitive decline and Alzheimer’s disease.8 High homocysteine by itself is considered a strong independent risk factor for dementia and Alzheimer’s disease. A study looking at data collected from the Framingham Study showed that a homocysteine level over 14 μmol/L increased the risk of developing Alzheimer’s disease by 150 percent.9

Bone Fractures

Homocysteine is considered an independent risk factor for osteoporosis fractures in the elderly.10 It is thought that homocysteine leads to fractures in the same way in which it contributes to heart disease in that homocysteine affects certain connective tissue proteins and prevents them from functioning correctly. In the case of fractures, homocysteine interferes with the cross-linking ability of collagen (a major connective tissue protein) with the tissues it supports such as the skeletal system. Because homocysteine affects the structural proteins of which bone is comprised, it does not actually affect bone density. Therefore, traditional measures used to build bones (weight bearing exercise, adequate calcium and vitamin D, etc.) will not necessarily correct the damage from homocysteine on the bones.

Controlling Elevated Homocysteine

homocysteine Homocysteine and OsteoporosisCurrently, there is no standard recommendation that all people have their homocysteine levels checked. Despite this, the American Heart Association does encourage testing for homocysteine in people with a personal or family history of heart disease. In order to address all possible aspects of heart disease (and other conditions), testing homocysteine levels is a good idea.

Controlling homocysteine can be achieved by supplementing with 4 common nutrients: vitamins B6, B12, folic acid and betaine. Vitamins B6, B12, and folic acid blood levels are found to be inversely related to plasma homocysteine concentration. Combination therapy with the aforementioned vitamins provides an effective way to reduce homocysteine levels,11 and side effects of this therapy are relatively unknown.12 Another supplement that has demonstrated usefulness in lowering homocysteine levels is betaine, also known as trimethylglycine.

High dietary consumption of methionine, which can be found in meats and dairy products, can result in the overproduction of homocysteine. Once homocysteine is produced it is metabolized in the body through one of two possible pathways—remethylation or transsulfuration. Remethylation is a process that utilizes folate, vitamin B12 or betaine (trimethylglycine) to convert homocysteine back to methionine. Alternately, transsulfuration utilizes vitamin B6 (pyridoxal-5-phosphate) to break down excess homocysteine into a number of metabolites for eventual excretion from the body.13,3 B6 has been shown to be effective in reducing homocysteine levels following the ingestion of significant amounts of methionine.14

Vitamin B12 in the form of methylcobalamin is needed for the conversion (remethylation) of homocysteine back to methionine.15 This remethylation reaction also requires folic acid. B12 is thought to provide an additive effect to the lowering of homocysteine when supplied in conjunction with folic acid.16

Folic acid is needed for the metabolism of homocysteine; low levels of folate in the blood are associated with higher levels of homocysteine. Folic acid is involved in one of the two pathways (remethylation) by which homocysteine is metabolized; this pathway also requires vitamin B12. Enzymes involved in remethylation of homocysteine are dependent upon folate and vitamin B12.17-18 Supplementation with folic acid will increase the activity of the remethylation pathway and thereby reduce homocysteine levels.19

Betaine is derived from choline and occurs naturally in the body. It can also be found in foods like cereal, seafood, spinach and beets, to name a few. Betaine acts as a methyl donor and contributes in the remethylation pathway when converting homocysteine back to methionine,20 thereby reducing homocysteine levels. Betaine has been shown to lower homocysteine levels in the majority of patients unresponsive to vitamin B6 therapy. In one study, daily doses of 250 mg of vitamin B6, 5 mg of folic acid, and 6 gm of betaine by themselves or in combination normalized the majority of high homocysteine levels in patients administered high doses of methionine.21

Homocysteine-lowering strategies also include a diet low in methionine since homocysteine is an intermediate product of methionine metabolism in the body. Foods rich in methionine include cheddar cheese, eggs, chicken, and beef.

Conclusion

Homocysteine is considered a primary, independent risk factor for cardiovascular disease and is thought to contribute to a host of other conditions such as miscarriages and difficult pregnancy, bone fractures, strokes, blood clots, depression, dementia, Alzheimer’s and Parkinson’s diseases. Due to this amino acid’s role in a host of diseases, individuals at risk for high homocysteine levels should consider a supplement regimen that includes vitamins B12 and B6, folic acid, and betaine.

References

1. Blum A, Hijazi I, Eizenberg MM, Blum N. Homocysteine (Hcy) follow-up study. Clin Invest Med. 2007;30(1):21-5.

2. Lentz SR. Mechanisms of homocysteine-induced atherothrombosis. J Thromb Haemost. 2005 Aug;3(8):1646-54.

3. Keebler ME, De Souza C, Fonesca V. Diagnosis and treatment of hyperhomocysteinemia. Curr Atheroscler Rep. 2001;3:54-63.

4. Boushey CJ, Beresford SA, Omenn GS, Motulsky AG. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease. Probable benefits of increasing folic acid intakes. JAMA. 1995;274:1049-57.

5. D’Uva M, Di Micco P, Strina I, et al. Hyperhomocysteinemia in women with unexplained sterility or recurrent early pregnancy loss from Southern Italy: a preliminary report. Thromb J. 2007 Jul 11;5:10.

6. Forges T, Monnier-Barbarino P, Alberto JM, et al. Impact of folate and homocysteine metabolism on human reproductive health. Hum Reprod Update. 2007 May-Jun;13(3):225-38. Epub 2007 Feb 16.

7. Herrmann W, Lorenzl S, Obeid R. Review of the role of hyperhomocysteinemia and B-vitamin deficiency in neurological and psychiatric disorders–current evidence and preliminary recommendations] Fortschr Neurol Psychiatr. 2007 Sep;75(9):515-27.

8. Rosendorff C, Beeri MS, Silverman JM. Cardiovascular risk factors for Alzheimer’s disease. Am J Geriatr Cardiol. 2007 May-Jun;16(3):143-9.

9. Seshadri S, Beiser A, Selhub J, et al. Plasma homocysteine as a risk factor for dementia and Alzheimer’s disease. N Engl J Med. 2002 Feb 14;346(7):476-83.

10. Perier MA, Gineyts E, Munoz F, Sornay-Rendu E, Delmas PD. Homocysteine and fracture risk in postmenopausal women: the OFELY study. Osteoporos Int. 2007 Oct;18(10):1329-36.

11. Krishnaswamy K, Lakshmi AV. Role of nutritional supplementation in reducing the levels of homocysteine. J Assoc Physicians India 2002 May;50 Suppl:36-42.

12. O’Connor JJ, Meurer LN. Should patients with coronary disease and high homocysteine take folic acid? J Fam Pract. 2003 Jan;52(1):16-8.

13. Sunder-Plassmann G, Winkelmayer WC, Fodinger M. Therapeutic potential of total homocysteine-lowering drugs on cardiovascular disease. Exp Opin Invest Drugs. 2000;9:2637-51.

14. Mayer EL, Jacobsen DW, Robinson K. Homocysteine and coronary atherosclerosis. J Am Coll Cardiol. 1996;27:517-27.

15. Selhub J, Jacques PF, Bostom AG, et al. Relationship between plasma homocysteine and vitamin status in the Framingham study population. Impact of folic acid fortification. Publ Health Rev. 2000;28:117-45.

16. Landgren F, Israelsson B, Lindgren A, et al. Plasma homocysteine in acute myocardial infarction: homocysteine-lowering effect of folic acid. J Intern Med. 1995;237:381-8.

17. Woodside JV, Yarnell JW, McMaster D, et al. Effect of B-group vitamins and antioxidant vitamins on hyperhomocysteinemia: a double-blind, randomized, factorial-design, controlled trial. Am J Clin Nutr. 1998;67:858-66.

18. Fohr IP, Prinz-Langenohl R, Bronstrup A, et al. 5,10-Methylenetetrahydrofolate reductase genotype determines the plasma homocysteine-lowering effect of supplementation with 5-methyltetrahydrofolate or folic acid in healthy young women. Am J Clin Nutr. 2002;75:275-82.

19. Vermeulen EG, Stehouwer CD, Twisk JW, et al. Effect of homocysteine-lowering treatment with folic acid plus vitamin B6 on progression of subclinical atherosclerosis: a randomised, placebo-controlled trial. Lancet. 2000;355:517-22.

20. Brouwer IA, Verhoef P, Urgert R. Betaine supplementation and plasma homocysteine in healthy volunteers (letter). Arch Intern Med. 2000;160:2546-7.

21. Boers GHJ. Hyperhomocystinemia: A Newly Recognized Risk Factor For Vascular Disease. Netherlands Journal of Medicine. 1994; 45:34-41.

No responses yet

Jun 16 2008

Published by under Anti Aging - Hormones

No responses yet

Jun 16 2008

Vitamin D3 – Osteoporosis

Published by under Osteoporosis,Vitamin D3

Vitamin D3:
Higher Doses Reduce Risk of Common Health Concerns
By Chris D. Meletis, ND

Vitamin D3 is one of the most useful nutritional tools we have at our disposal for improving overall health. This vitamin is unique because cholecalciferol (Vitamin D3) is a vitamin derived from 7-dehyrocholesterol; however, Vitamin D3 acquires hormone-like actions when cholecalciferol (Vitamin D3) is converted to 1,25-dihydroxy Vitamin D3 (Calcitriol) by the liver and kidneys. As a hormone, Calcitriol controls phosphorus, calcium, and bone metabolism and neuromuscular function. Vitamin D3 is the only vitamin the body can manufacture from sunlight (UVB). Yet, with today’s indoor living and the extensive use of sunscreens due to concern about skin cancer, we are now a society with millions of individuals deficient in life-sustaining bone building and immune modulating 1,25-dihydroxy Vitamin D3.

For more than a century, scientists have recognized that Vitamin D3 is involved in bone health. Research has continued to accumulate, documenting Calcitriol’s role in the reduction of the risk of fractures to a significant degree. The latest research, however, shows that 1,25-dihyroxy Vitamin D3 deficiency is linked to a surprising number of other health conditions such as depression, back pain, cancer, both insulin resistance and pre-eclampsia during pregnancy, impaired immunity and macular degeneration.

As it becomes clear that Vitamin D3 plays a wide role in overall health, it’s becoming equally clear that a large percentage of individuals are deficient in this important nutrient, which has hormone-like activity. The fear of skin cancer has stopped many individuals from obtaining beneficial amounts of sunlight. The skin uses the energy of UVB to convert 7-dehydrocholesterol into Vitamin D3. Even individuals, who venture out into the sun often and use suntan lotion, may be deficient in Vitamin D3. Furthermore, as we age, we are less equipped to produce sufficient quantities of this vital nutrient. One study found that age-related declines in kidney function may require older people to ingest more Vitamin D3 to maintain the same blood levels as younger people.1

The Recommended Daily Intake (RDI) of Vitamin D3 is set so low those mature individuals who consume this small amount (400 to 600 International Unites (I.U.’s)) are still likely to be deficient if they live north of the Tropic of Cancer or south of the Tropic of Capricorn. In fact, researchers have discovered that the RDI, which was considered adequate to prevent osteomalacia (a painful bone disease) or rickets, is not high enough to protect against the majority of diseases linked to 1,25-dihyroxy Vitamin D3 deficiency. For example, an analysis of the medical literature found that at least 1,000 to 2,000 IU of Vitamin D3 per day is necessary to reduce the risk of colorectal cancer and that lower doses of Vitamin D3 did not have the same protective effect.2

Researchers Call for Higher Doses

In an editorial in the March 2007 edition of the American Journal of Clinical Nutrition, a prominent group of researchers from leading institutions such as the University of Toronto, Brigham and Women’s Hospital, Tufts University and University Hospital in Zurich, Switzerland, lashed out at the conventional media for its inaccurate reporting of Vitamin D supplementation.3

The researchers wrote, “Almost every time the public media report that Vitamin D nutrition status is too low, or that higher Vitamin D intakes may improve measures of health, the advice that accompanies the report is outdated and thus misleading. Media reports to the public are typically accompanied by a paragraph that approximates the following: ‘Current recommendations from the Institute of Medicine call for 200 IU/day from birth through age 50 years, 400 IU for those aged 51–70 years, and 600 IU for those aged >70 years. Some experts say that optimal amounts are closer to 1,000 IU daily. Until more is known, it is wise not to overdo it.’ The only conclusion that the public can draw from this is to do nothing different from what they have done in the past.”

The researchers point out that supplemental intake of 400 IU per day barely raises blood concentrations of 25(OH)D, which is the circulating Vitamin D metabolite that serves as the most frequently measured indicator of Vitamin D status. To raise 25(OH)D from 50 to 80 nmol/L requires an additional intake of 1,700 IU Vitamin D per day.

The researchers went on to write that, “The balance of the evidence leads to the conclusion that the public health is best served by a recommendation of higher daily intakes of Vitamin D. Relatively simple and low-cost changes, such as increased food fortification or increasing the amount of Vitamin D in Vitamin supplement products, may very well bring about rapid and important reductions in the morbidity associated with low Vitamin D status.”

One of the challenges is the outdated acceptable upper limit for Vitamin D3 consumption, which was set at 2,000 IU. However, researchers point out that more recent studies have shown that 10,000 IU is the safe upper limit.4

Dr. R. Vieth, one of the foremost authorities on Vitamin D3 supplementation, has extensively studied Vitamin D, and lamented the low requirements for Vitamin D3 in a recent issue of the Journal of Nutrition: “Inappropriately low UL [upper limit] values, or guidance values, for Vitamin D have hindered objective clinical research on Vitamin D nutrition; they have hindered our understanding of its role in disease prevention, and restricted the amount of Vitamin D in multivitamins and foods to doses (that are) too low to benefit public health.”5

When examining the medical literature, it becomes clear that Vitamin D3 affects human health in an astonishing number of ways and that not obtaining enough of this important nutrient can leave the door open to developing a number of health conditions.

Depression

Vitamin D3 deficiency is common in older adults and has been implicated in psychiatric and neurologic disorders. For example, in one study of 80 older adults (40 with mild Alzheimer’s disease and 40 nondemented persons), Vitamin D3 deficiency was associated with low mood and with impairment on two of four measures of cognitive performance.6

Back Pain

Musculoskeletal disorders have been linked to Vitamin D3 deficiency in a number of studies. One of the newest studies explored the role that low Vitamin D3 levels play in the development of chronic low back pain in women. Sixty female patients in Egypt complaining of low back pain lasting more than three months were studied. Researchers measured levels of Vitamin D3 in the women with low back pain and compared those levels to those of 20 matched healthy controls.

The study revealed that patients with low back pain had significantly lower Vitamin D3 levels than controls. Low Vitamin D3 levels (25 OHD < 40 ng/ml) were found in 49/60 patients (81 percent) and 12/20 (60 percent) of controls.7

Bone Health

One of the best known and long-established benefits of Vitamin D3 is its ability to improve bone health and the health of the musculoskeletal system. It is well documented that Vitamin D3 deficiency causes osteopenia, precipitates and exacerbates osteoporosis, causes a painful bone disease known as osteomalacia, and exacerbates muscle weakness, which increases the risk of falls and fractures. Vitamin D3 insufficiency may alter the regulatory mechanisms of parathyroid hormone (PTH) and cause a secondary hyperparathyroidism that increases the risk of osteoporosis and fractures.8

Cognitive Enhancement

Scientists are developing a greater appreciation for Vitamin D3’s ability to improve cognition. In a recent study, Vitamin D3 deficient subjects scored worse on mental function tests compared to individuals who had higher levels of the Vitamin.9 The researchers wrote, “In conclusion, the positive, significant correlation between serum 25(OH)D concentration and MMSE [mental state examination scores] in these patients suggests a potential role for Vitamin D in cognitive function of older adults.”

Cancer

One researcher first noted the connection between Vitamin D3 and protection from cancer in the 1940s, when he discovered that individuals at sunny latitudes had a reduced rate of deaths from cancer. He suggested that sunlight provided “a relative cancer immunity.”
Since then, a number of studies have strongly suggested that Vitamin D3 deficiency is associated with an increased risk of developing many forms of cancer including breast, ovarian, prostate and colon cancer.10 In one recent clinical trial, researchers studied 1,179 healthy, postmenopausal women (all 55 years or older and free of known cancers for at least 10 years prior to entering the study) who were taking large amounts of Vitamin D3 with calcium. The subjects were randomly assigned to take daily dosages of: (1) 1,400-1,500 mg supplemental calcium, (2) 1,400-1,500 mg supplemental calcium plus 1,100 IU of Vitamin D3, or (3) placebos. Over the four-year trial, women in the calcium/Vitamin D3 group experienced a 60 percent or greater reduced risk of cancer than their peers in the placebo group, who were not consuming these supplements.

Because there was the chance that some women may have had undiagnosed cancers at the study’s start, the researchers threw out the first-year results and then analyzed the results from the last three years of the trial. These later years resulted in even more dramatic decrease, with the calcium/Vitamin D3 group experiencing a 77 percent reduction in cancer risk.

There was no statistically significant difference in cancer incidence between the participants taking placebos and subjects consuming only calcium supplements.11

Another interesting study demonstrated that in vitro Vitamin D3 may cause tumor cells to be more sensitive to chemotherapy drugs, increasing the efficacy of the cancer treatment.12

Immunity

Scientists have linked various aspects of immune health to a Vitamin D3 deficiency. Vitamin D3 regulates T cells, which are important to the functioning of a strong immune system. Vitamin D3 acts as an immune system modulator, preventing excessive expression of inflammatory cytokines and increasing the killing efficiency of macrophages. In addition, it dramatically stimulates the expression of potent anti-microbial peptides, which exist in immune system cells such as neutrophils, monocytes, natural killer cells, and in cells lining the respiratory tract. These Vitamin-D3-stimulated peptides play a major role in protecting the lung from infection.13

In addition, Vitamin D3 deficiency may influence development and progression of various autoimmune diseases.14

Multi-Talented Nutrient

Vitamin D3 deficiency has been linked to a host of other conditions such as high blood pressure, fibromyalgia, diabetes, multiple sclerosis, rheumatoid arthritis, and an increased risk of pre-eclampsia and insulin resistance during pregnancy.11,15-16 Most recently, low Vitamin D3 levels have been linked to an increased prevalence of early age-related macular degeneration.17

Proper Dosage

In many of my patients, even after consuming 2,000 to 4,000 IU of Vitamin D3 per day, their test results indicate that their Vitamin D3 levels have not increased. These patients needed to consume 8,000 IU of Vitamin D3 per day to achieve proper blood levels of the Vitamin. Patients should, therefore, have their physicians test their serum 1,25-dihyroxy D3 levels to determine the proper level of supplementation required. Testing is very important due to the fact that, in a small number of patients, Vitamin D3 supplementation can raise calcium levels to an excessively high level. I have found this to be especially true in African American patients. Testing for 1,25-dihyroxy Vitamin D3, PTH and calcium blood levels should therefore become a part of every woman’s regular blood work.

Conclusion

A growing number of researchers who have widely studied Vitamin D3 are almost begging the general public to consume more of this important nutrient. Due to Vitamin D3’s high safety profile in doses up to 10,000 IU per day and because of the wide role it plays in our health, consuming 2,000 to 4,000 IU per day of this nutrient at times of the year when sunlight is scarce is a prudent way to improve overall health.

References

1. Vieth R, Ladak Y, Walfish PG. Age-related changes in the 25-hydroxyVitamin D versus parathyroid hormone relationship suggest a different reason why older adults require more Vitamin D. J Clin Endocrinol Metab. 2003 Jan;88(1):185-91.
2. Gorham ED, Garland CF, Garland FC, Grant WB, Mohr SB, Lipkin M, Newmark HL, Giovannucci E, Wei M, Holick MF. Optimal Vitamin D status for colorectal cancer prevention: a quantitative meta analysis. Am J Prev Med. 2007 Mar;32(3):210-6.
3. Vieth R, Bischoff-Ferrari H, Boucher BJ, Dawson-Hughes B, Garland CF, Heaney RP, Holick MF, Hollis BW, Lamberg-Allardt C, McGrath JJ, Norman AW, Scragg R, Whiting SJ, Willett WC, Zittermann A. The urgent need to recommend an intake of Vitamin D that is effective. American Journal of Clinical Nutrition. March 2007;85(3):649-650.
4. Hathcock JN, Shao A, Vieth R, Heaney R. Risk assessment for Vitamin D. Am J Clin Nutr. 2007 Jan;85(1):6-18.
5. Vieth R. Critique of the considerations for establishing the tolerable upper intake level for Vitamin D: critical need for revision upwards. J Nutr. 2006 Apr;136(4):1117-22.
6. Wilkins CH, Sheline YI, Roe CM, Birge SJ, Morris JC. Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults. Am J Geriatr Psychiatry. 2006 Dec;14(12):1032-40.
7. Lotfi A, Abdel-Nasser AM, Hamdy A, Omran AA, El-Rehany MA. HypoVitaminosis D in female patients with chronic low back pain. Clin Rheumatol. 2007 Mar 22; [Epub ahead of print].
8. Pérez-López FR. Vitamin D and its implications for musculoskeletal health in women: An update. Maturitas. 2007 Jun 28; [Epub ahead of print].
9. Przybelski RJ, Binkley NC. Is Vitamin D important for preserving cognition? A positive correlation of serum 25-hydroxyVitamin D concentration with cognitive function. Arch Biochem Biophys. 2007 Apr 15;460(2):202-5.
10. Grant WB. An estimate of premature cancer mortality in the U.S. due to inadequate doses of solar ultraviolet-B radiation. Cancer. 2002 Mar 15;94(6):1867-75.
11. Lappe J, Travers-Gustafson D, Davies K, Recker R, Heaney R. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. American Journal of Clinical Nutrition. June 8;85(6):1586-1591.
12. Ma Y, et al. Study presented at the 2007 centennial meeting of the American Association for Cancer Research (AACR), April 14 to 18, 2007, Los Angeles.
13. Cannell JJ, Vieth R, Umhau JC, Holick MF, Grant WB, Madronich S, Garland CF, Giovannucci E. Epidemic influenza and Vitamin D. Epidemiol Infect. 2006 Dec;134(6):1129-40.
14. Kuryłowicz A, Bednarczuk T, Nauman J. [The influence of Vitamin D deficiency on cancers and autoimmune diseases development.] [Article in Polish] Endokrynol Pol. 2007;58(2):140-152.
15. Bodnar LM, Catov JM, Simhan HN, Holick MF, Powers RW, Roberts JM. Maternal Vitamin D deficiency increases the risk of preeclampsia. J Clin Endocrinol Metab. 2007 May 29; [Epub ahead of print].
16. Maghbooli Z, Hossein-Nezhad A, Karimi F, Shafaei AR, Larijani B. Correlation between Vitamin D(3) deficiency and insulin resistance in pregnancy. Diabetes Metab Res Rev. 2007 Jul 2; [Epub ahead of print].
17. Parekh N, Chappell RJ, Millen AE, Albert DM, Mares JA. Association Between Vitamin D and Age-Related Macular Degeneration in the Third National Health and Nutrition Examination Survey, 1988 Through 1994. Arch Ophthalmol. May 2007;125: 661-669.

No responses yet

Jun 13 2008

Anabolic Hormone Depletion is Common in Men with Chronic Heart Failure

In a study involving 208 men with chronic heart failure (median age: 63 years) and 366 healthy controls, anabolic hormone depletion was found to be quite prevalent among men with chronic heart failure, and was found to be associated with poor prognostic consequences. Immunoassays were used to measure levels of various hormones in subjects. Results found that men of all ages with chronic heart failure were found to have deficiencies in DHEAS, circulating total testosterone (TT), estimated free testosterone (eFT), and insulin-like growth factor-1 (IGF-1). Furthermore, DHEAS, TT, and eFT were found to be inversely associated to New York Heart Association class. After adjusting for established prognostic factors, all four hormones were found to be prognostic markers as well. A positive association was found between DHEAS and left ventricular ejection fraction. Men with chronic heart failure but normal anabolic hormone levels had the best 3-year survival rates compared to those having deficiencies in one, two, or all three anabolic endocrine axes (74%, 55%, and 27%, respectively). These results suggest that men with chronic heart failure who have a deficiency in more than one anabolic hormone may have an increased risk of mortality.

Reference: “Anabolic deficiency in men with chronic heart failure: prevalence and detrimental impact on survival,” Jankowska EA, Biel B, et al, Circulation, 2006; 114(17): 1829-37. (Address: Cardiology Department, Military Hospital, ul. Weigla 5, 50-981 Wroclaw, Poland. E-mail: Ewa.Jankowska@antro.pan.wroc.pl ).

No responses yet

Jun 10 2008

Scientists Propose Mechanism Behind Niacin’s Ability to Raise “Good” Cholesterol Breaking News

A new study investigating the mechanism by which niacin is able to raise HDL, the “good” cholesterol, has found that the B vitamin may exert its effects on the liver by inhibiting the excretion of HDL.

Niacin is known to increase plasma HDL levels, but the mechanism by which niacin exerts its action is not clearly understood. Therefore, scientists undertook a new study to clarify exactly how niacin is able to raise HDL.

In the body, a substance called “a beta chain” takes up HDL and therefore reduces the level of good cholesterol. Researchers investigated niacin’s effects on beta-chain’s ability to uptake HDL, by incubating human liver cells with niacin. When they did this a 27 percent reduction in the presence of beta chains on the cell surface was observed. Furthermore, the scientists observed a 35 percent reduction in the uptake of HDL in cells treated with niacin.

The results of the in vitro study suggested that niacin stops the liver from removing HDL from the blood, allowing the body to preserve its high plasma HDL levels.

Griffin Medical Group prescribes pharmaceutical sustained release niacin (generic Niaspan) to raise HDL levels. Starting dose is 500mg each day with food. This product may cause a flushing episode that can last up to 30 minutes. This flushing will subside over time with continued use. You may want to take SR Niacin with ½ an aspirin to control the flushing during the initial phase of treatment.

Click here to order

Reference:

Zhang LH, Kamanna VS, Zhang MC, Kashyap ML. Niacin inhibits surface expression of ATP synthase {beta} chain in HepG2 cells: implications for raising HDL. J Lipid Res. 2008 Jun;49(6):1195-201.

Yours in health,

Griffin Medical Group

www.griffinmedical.com

No responses yet

Jun 10 2008

Testosterone Supplementation Decreases Metabolic Syndrome and Improves Sexual Function

Reports on hormones findings from F. Saad and co-researchers

“Administration of testosterone cypionate over 12 months to men with sexual dysfunction and signs of the metabolic syndrome, restored their plasma testosterone (T) levels to the mid-range of reference values. This had a beneficial effect on their sexual functioning as evidenced by an improvement of their scores on the International Index of Erectile Function,” researchers in Berlin, Germany report (see also Hormones).
“The scores on the Aging Male Symptoms score, AMS, were also improved. Most impressive were the improvements in the parameters of the metabolic syndrome; they all improved and appeared largely correlated (i.e., decline in waist circumference with declines of plasma cholesterol and LDL and increase in plasma HDL). Sex hormone binding globulin, SHBG, may be considered as an indicator of the severity of the metabolic syndrome; levels of SHBG initially fell, probably as a result of rising plasma T levels. But over the last six months of the observation period when plasma T rose further, there was a significant increase in plasma SHBG which may be interpreted to indicate an improvement of the metabolic syndrome. Blood pressure improved slightly but significantly. in this cohort of elderly men (54-76 years; median 64 years) there were no safety concerns over a one year period of T administration. Prostate specific antigen, PSA, levels remained stable; the International Prostate Symptoms Score, IPSS, improved slightly. Liver functions and plasma glucose remained stable,” wrote F. Saad and colleagues.

The researchers concluded: “Hemoglogin and hematocrit values increased but remained within reference values.”

Yours in health,

Griffin Medical Group

www.griffinmedical.com

No responses yet

Jun 04 2008

New hints seen that the antioxidant component of red wine (resveratrol) slows aging

Wednesday, June 4, 2008

Red wine is much more potent than was thought in extending human lifespan, researchers say in a new report that is likely to give impetus to the rapidly growing search for longevity drugs.

The study is based on dosing mice with pharmaceutical resveratrol, an ingredient of some red wines. Some scientists are already taking pharmaceutical resveratrol in capsule form.

The report is part of a new wave of interest in drugs that may enhance longevity. On Monday, Sirtris, a startup founded in 2004 to develop drugs with the same effects as resveratrol, completed its sale to GlaxoSmithKline for $720 million. Continue Reading »

No responses yet

Jun 04 2008

The Deadly Truth About Diabetes


The Thin Man’s Diabetes

America‘s fastest-growing disease has a sugar-coated secret: You don’t need to be overweight for it to kill you

By: Jeff O’Connell

One of my most enduring childhood images is from a newspaper clipping. The grainy photograph freezes a lanky teen named Tom O’Connell launching a hook shot from his right thigh. Tucker, as he was known, led a team from tiny Merchantville High School in scoring and rebounding during an improbable run to the South Jersey Championship. New Jersey had its own version of Hoosiers in 1952, and for that one season, my father was his team’s Jimmy Chitwood.

Continue Reading »

No responses yet

Jun 03 2008

Nettle Root

Published by under Vitamins & Supplements

The roots of the stinging nettle are useful for male hormone balance. Extracts known as lignans derived from the roots have the ability to bind sex hormone binding globulin (SHBG). When SHBG is bound, this may allow for more unbound, or free (bioavailable) testosterone to be available for biological processes and this may prevent SHBG from binding to the prostate gland, which may prevent prostatic enlargement via SHBG binding 5. Bioavailable testosterone represents the fraction of circulating testosterone that readily enters cells and better reflects the bioactivity of testosterone. The better bioactivity means a more healthful benefit from testosterone.1 Stinging nettle root constituents also act to control the growth of prostatic cells and resultant symptoms.2-3 Nettle root also contains another constituent known as beta-sitosterol which has positive effects on testosterone levels and prostate health.4

Griffin Medical Group recommends 250mg twice a day between meals which may allow more free testosterone.

Yours in health,

Griffin Medical Group

www.griffinmedical.com

1. Hyrb D et al. The effect of extracts of the roots of the stinging nettle (Urtica dioca) on the interaction of SHBG with its receptor on human prostatic membranes. Planta Med, 1995, 61:31-32.
2. Konrad L, Muller HH, Lenz C, et al. Antiproliferative effect on human prostate cancer cells by a stinging nettle root (Urtica dioica) extract. Planta Med 2000;66:44-7.
3. Lichius JJ, Muth C. The inhibiting effects of Urtica dioica root extracts on experimentally induced prostatic hyperplasia in the mouse. Planta Med 1997;63:307-10.
4. Durak I, Biri H, Devrim E, et al. Aqueous extract of Urtica dioica makes significant inhibition on adenosine deaminase activity in prostate tissue from patients with prostate cancer. Cancer Biol Ther 2004;3:855-7.
5. Schottner M, Gansser D, Spiteller G, et al. Lignans from the roots of Urtica dioica and their metabolites bind to human sex hormone binding globulin (SHBG). Planta Med 1997;63:529-32.

No responses yet

May 21 2008

Age Management or Anti Aging Medicine – By Dr. Judi Goldstone

Published by under Anti Aging - Hormones

It is no longer necessary to accept the mental and physical decline associated with aging. A century ago the average life expectancy was 43 to 47. Today, life expectancy has almost doubled, due mostly to advances in medicine and technology. The rapid rate of these advances may put one in position to take advantage of cutting edge technologies in the pipeline, such as genetic engineering, stem cell transplants, therapeutic cloning, nanotechnology, and artificial organs. However, a longer life span is only desirable if living longer means living stronger, healthier, and without disabilities.
This is the premise of Anti-Aging Medicine, which is also known as Age Management Medicine, Longevity Medicine, Preventive-Regenerative Medicine, or Optimal Aging Medicine. Preventive-Regenerative Medicine is a new specialty of heath care based on early detection, prevention, and reversal of the degenerative effects of aging. The primary goal is living healthier for a longer period of time. The Anti-Aging specialty began in 1993 when twelve forward thinking physicians formed the American Academy of Anti-Aging Medicine (A4M). Today, the Academy is composed of 20,000 physicians and scientists from over 70 countries. It is the fastest growing scientific society in the world. The Academy is devoted to examining scientific research pertaining to: the causes of illness; aging; and the decline in physical and mental function as aging occurs. The principals of Preventive-Regenerative Medicine are well documented in medical and scientific journals, and are based on sound and responsible medical care.
Research suggests that aging is likely due to a combination of causes. Some theories of aging include: degeneration of bodily functions due to hormone decline, free radical damage due to lifestyle factors, chronic inflammation, loss of DNA’s ability to reproduce, or too much insulin. When these events are controlled or prevented, the likelihood of illness and disability is reduced or prevented, and it becomes possible to maintain good general health, strong muscles and bones, an efficient immune system, sharp memory, and peak mental and physical function at any age. While traditional medicine focuses on treating the effects of the aging process, Anti- Aging Medicine focuses on treating or preventing the causes of aging. Stated differently, traditional medicine predominately treats external symptoms that have internal causes, while Anti-Aging Medicine addresses the internal causes in order to prevent external symptoms. The different approach may sound subtle, but it can produce substantial differences in a person’s health and well being.
How does Preventive-Regenerative Medicine produce these results? At Griffin Medical Dr. Goldstone customizes a program for each individual after performing a physical exam, obtaining a comprehensive medical history, and conducting a nutritional and fitness evaluation. In addition, Dr. Goldstone obtains an advanced blood analysis, that includes blood count, body chemistries, blood sugar, organ function, hormone levels, cardiovascular and cancer risk factors, and inflammatory markers. She then designs a program based on replacement of deficient hormones and neutraceuticals, exercise, stress reduction, diet, and inflammation control. Bio-identical hormones (i.e., identical to human hormones) are used when replacement is necessary. Hormone levels are restored to a youthful range, and the patient’s progress is regularly monitored by physical exam and lab work, typically every three months for the first year, and every six to twelve months the reafter.
Judi Goldstone, MD is California native and a cum laude graduate of the University of California at Los Angeles. She received her medical degree from Mount Sinai School of Medicine in New York, where she graduated in the top third of her class. She is certified by the American Board of Internal Medicine and has been practicing internal medicine in Southern California most of her career. For the past 8 years Dr Goldstone began practicing bariatric(weight loss) and wellness medicine. She is an active member of the American Society of Bariatric Physicians and the American Academy of Antiaging and Regenerative Medicine. Dr. Goldstone has extensive experience in bio identical hormone replacement therapy, growth hormone replacement, menopause, andropause (male menopause), neutraceutical supplementation, nutrition, and weight loss.

No responses yet

May 21 2008

Quality Assurance Alert – Toxic Chemicals in Raw Materials

As you know by now, Griffin Medical Group only prescribes pharmaceutical vitamins and supplements. We are one of only a few medical groups that seek quality in all the products we recommend. We feel that we are the leader in quality assurance. Contamination in natural products is a huge issue, whether the material comes from China, India, Europe or the United States. It is not where the material comes from that matters, but how thoroughly it was tested for purity before it gets put into a product and sold. Here are a few of the solvent tainted raw materials that we have been advised of by the pharmaceutical companies we work with. The following raw materials were deemed unacceptable to pharmaceutical supplement companies. Continue Reading »

One response so far

May 21 2008

Vitamin D3 Important for Male and Female Health

Published by under Vitamin D3

Two recent studies indicate higher levels of vitamin D are associated with a reduced risk of breast and prostate cancer.

In the newest of the two studies, researchers investigated the relationship between serum 25-hydroxyvitamin D [25(OH)D] levels (a measurement of vitamin D3 levels in the body) and the incidence rates of breast cancer in 107 countries. The researchers also looked at the number of breast cancer cases that occurred at varying latitudes since past studies have found lower breast cancer rates in areas that receive higher amounts of sunlight. The lower breast cancer rate in these areas is thought to be attributable to the fact that the skin makes vitamin D from sunlight. Continue Reading »

No responses yet

May 08 2008

D-Ribose and Creatine Increase Mitochondrial Energy Production

Published by under Creatine - Whey,D-Ribose

A series of recent articles in Vitamin Research News have examined aspects of the Mitochondrial-Free Radical Theory of Aging, describing how the declining function of mitochondria— the tiny organelles responsible for producing ATP— contribute to aging and the diseases of aging. Additionally, the articles outlined a number of nutritional approaches aimed at restoring functional performance to aging mitochondria to increase their ability to produce ATP at more youthful levels.
Here we present additional substances that are also proven to enhance mitochondrial oxidative phosphorylation and energy production. These include:

D-Ribose—Energy Producing ATP Substrate
Ribose is a naturally occurring 5-carbon sugar produced in the body from glucose (Fig. 1). In addition to serving as the carbohydrate backbone for ribonucleic acid (RNA) and deoxyribonucleic acid (DNA), ribose is also an essential ingredient in the manufacture of ATP. The mitochondria found in high-energy-output organs—such as the heart, liver, adrenals, GI tract, brain, muscles and endocrine glands—utilize two methods for building or conserving cyclic nucleotides like ATP, ADP, and AMP.
The first process by which these nucleotides are synthesized is the de novo pathway, in which nucleotides are made “from scratch,” starting with ribose. This is the slower of the two pathways.
The second, faster pathway, is the salvage pathway, in which the mitochondria “pick up the pieces” of ATP metabolites to form new ATP. In this manner ribose enables the cells to quickly and efficiently recycle (i.e., salvage) the end products formed by the breakdown of ATP to form new ATP molecules. Thus, this is known as the salvage pathway of ATP formation.
Ribose is essential for both the salvage and de novo reactions to work. Ribose is formed in the body from glucose, through a process known as the pentose phosphate pathway (Fig. 2). Aside from this relatively time-consuming pathway, there are no foods able to provide enough ribose to rapidly restore ribose levels, should the need arise, as when exercising or working, and especially during a heart attack or stroke.

Restoring Ribose Levels
Scientists have found that oral or intravenous ribose can rapidly restore ribose levels in nerves and muscles. Ribose supplementation can dramatically improve recovery of failing ATP levels during and following acute or chronic anoxia or ischemia. Research has shown that taking ribose has a positive effect on ATP production in all muscle fiber types, especially the heart. Ribose supplementation increases the de novo production of ATP through oxidative phosphorylation by 340 to 430 percent. Ribose also activates the salvage pathway, causing nucleotides to be revitalized into the manufacture of ATP by over 700 percent.

Ribose and Cardiovascular Diseases
Dr. Wolfgang Pliml and colleagues in Germany demonstrated that oral administration of ribose is effective in increasing the heart’s tolerance to ischemia (reduced blood flow). Twenty patients diagnosed with coronary artery disease completed two treadmill tests on consecutive days to establish pain thresholds for each patient. The researchers then gave each patient 60 grams of ribose per day for three days, and administered another treadmill test. Patients supplemented with ribose were able to walk further before pain symptoms occurred than those given the placebo.1
In a second study, 12 patients diagnosed with unstable coronary artery disease and congestive heart failure were administered five grams of ribose, three times daily, for three weeks. Evaluation by pre- and post-ribose echocardiogram revealed improvement in many parameters, including stroke volume index, ejection fraction, and left ventricular systolic volume.2

Ribose and Athletic Performance
Ribose has also been shown to increase athletic performance. Supplementation (ten grams per day) in young male recreational bodybuilders resulted in significant increases in muscular strength and total work performance after four weeks, compared with pre-treatment levels. No changes were noted in those using a placebo.3
Another study of seven healthy men who performed two sessions of bicycle ergometry to exhaustion at a one-week interval indicated that ribose improved efficiency of energy production, as evidenced by reduction of oxidative stress during vigorous exercise. Prior to the second trial, the subjects ingested seven grams of ribose. Ribose ingestion resulted in a reduction of urinary MDA (an indicator of oxidative stress), and lower heart rates at the same intensity of exercise as compared to the unsupplemented group.4

Creatine—Energy Enhancing Supplement
Creatine is an essential, natural substance that is synthesized in the body from three amino acids: glycine, arginine, and methionine. Creatine plays a very powerful role in energy metabolism as a muscle fuel in its role in regenerating ATP.
Operating through the ATP/ADP cycle (Fig. 3), creatine phosphate maintains ATP levels by serving as a reservoir of high-energy phosphate bonds in muscle and nerve tissues. The energy required to rephosphorylate ADP into ATP depends on the amount of phosphocreatine (PCr) stored in muscle tissues. As phosphocreatine is depleted during exercise, energy availability declines due to a loss of ability to resynthesize ATP at the rate required.
While scientists have been aware of creatine since 1832, it was not tested as a performance-enhancing nutrient until 1943, when researchers learned that creatine supplementation extended the cycling times of athletes.5 This nearly-forgotten, single, isolated report languished in the medical literature for over 50 years. However, a number of studies have now corroborated this early study, showing that creatine enhances both strength and endurance in athletes. In one study, creatine was given to 25 football players who had reached a plateau while undergoing a weight-training program. After 28 days of supplementation with creatine, researchers measured a 41 percent increase in “lifting volume” (sum of all lifts).6
Another five-week study of 42 football players also showed gains in strength and mass,7 as did a study of 29 women who took supplemental creatine for ten weeks.8 Some researchers have shown strength gains with as little as five to seven days of supplementation.9,10

Creatine Increases Strength and Energy in Older Adults
Because older people have lower levels of energy-producing muscle phosphocreatine,11 researchers examined creatine to see if supplementation could help seniors overcome this deficit. Subsequent studies have demonstrated that supplemental intake of creatine can effectively increase the available “pool” of creatine stored in muscles and enhance the capacity of older subjects to produce phosphocreatine. In 1998 Smith and colleagues administered creatine to younger (average age, 30) and older (average age, 58) men and women, and then tested their ability to perform a leg exercise. Both older and younger subjects experienced increased muscular endurance. In addition, the phosphocreatine resynthesis rate (PCr) of the older subjects was restored to that of youthful adults (Fig. 4).12
Also in 1998, Rawson and colleagues at the University of Massachusetts demonstrated that five days of creatine administration to a group of older men resulted in a small increase in lean body mass, and a slight improvement in exercise performance.13 This short study was followed up by a larger (20 male subjects, ranging in age from 60-82) and longer (30 days) study in which the subjects were first given a loading dose (20 grams per day) for ten days, followed by four grams of creatine per day for 20 days.14 At the end of the study, six of the ten creatine users reported an increased feeling of muscle strength or less difficulty performing daily activities. Five subjects demonstrated an increase in body mass, three showed an increase in arm strength, and four demonstrated reduced leg fatigue. One subject increased in all three measures. The authors concluded modestly that creatine might have a beneficial effect on reducing muscle fatigue.
Scientists at the University of Saskatchewan conducted a double blind study of the effects of creatine and a weight training program in men over 70. They demonstrated a significant advantage of creatine over placebo in terms of increased lean body mass, reduction in body fat, and increased muscular strength, and endurance.15

Cardiovascular Benefits of Creatine
Creatine is not just of benefit to athletes. In a study of older men (ranging from 43 to 70 years) suffering from chronic heart failure, researchers noted improvements in exercise performance and increased muscle creatine and phosphocreatine levels after ten days’ ingestion of 20 grams of creatine each day.16
In Italy, physicians administered six grams of creatine each day to 13 patients hospitalized with congestive heart failure. After four days, they noted a reduction in heart size, reduced vascular resistance, and increased ejection fraction—all indicators of improved heart function.17

Neuroprotective Effects of Creatine
In a review article, Tarnopolsky concluded that creatine monohydrate supplementation results in an increase in skeletal muscle total and phosphocreatine concentrations, increased fat-free mass, and enhanced high-intensity exercise performance in young healthy men and women.18 He also noted “neuroprotective effects, which have been proposed to be of benefit in Parkinson’s disease, Alzheimer’s disease, ALS, and after ischemia.” He concluded that creatine appeared to have potential to attenuate age-related muscle atrophy and strength loss, as well as to protect against neurodegenerative disorders.
Shortly after Tarnopolsky’s review, FDA granted “orphan drug status” to creatine as a treatment for patients with amyotrophic lateral sclerosis (Lou Gehrig’s disease), based on creatine’s demonstrated ability to enhance cellular energy production. In addition, a European patent has also been issued for the use of creatine compounds to prevent aging effects and to treat muscle atrophy.19

Conclusion
Creatine and ribose, acting at the mitochondrial level, enhance muscular, cardiovascular, and neurological function. Although high optimal doses of creatine and ribose were used in many of the studies cited in this article, other researchers have shown that regular, long term use of lower doses may be equally effective. For greatest effect these substances should be consumed on a continuous basis (around the clock), and especially prior to high energy requirements.

References

1. Pliml, Wolfgang, Von Arnim, Thomas, Stablein, Alexander, et al. Effects of ribose on exercise-induced ischemia in stable coronary artery disease. The Lancet, 1992, 340, 507-510.
2. Illien, Steffan, Omran, H., MacCarter, D., and St. Cyr, J. Ribose improves myocardial function in congestive heart failure, FASEB Journal, 2001, 15: 5, A1142.
3. Van Gammeren, D., Falk, D., and Antonio, J. The effects of four weeks of ribose supplementation on body composition and exercise performance in healthy, young, male recreational body builders: A double-blind, placebo controlled trial. Current Therapeutic Research, 2002, 63: 8, 486-495.
4. Seifer, J.G., Subudhi, A., Fu, M.X., et al. The effects of ribose ingestion on indices of free radical production during hypoxic exercise, Free Radical Biology and Medicine, 2002, 33 (Suppl 1): S269.
5. Keys, A. Physical performance in relation to diet. Fed Proc, 1943, 2: 164.
6. Kreider, R.B., Ferreira, M., Wilsoln, M., et al. Effects of creatine supplementation on body composition, strength, and sprint performance. Med Sci Sports Exerc, 1998, 30: 73-82.
7. Stone, M.H., Sanborn, K., Smith, L.L., et al. Effects of in-season (5 weeks) creatine and pyruvate supplementation on anaerobic performance and body composition in American football players. Int J Sport Nutr, 1999, 9: 146-165.
8. Vandenberghe, K., Goris, M., Van Hecke, P, et al. Long-term creatine intake is beneficial to muscle performance during resistance training. J Appl Physiol, 1997, 83: 2055-2063.
9. Urbanski, R.L., Vincent, W.J., Yuaspelkis, B.B. Creatine supplementation differentially affects maximal isometric strength and time to fatigue in large and small muscle groups. Int J Sport Nutr, 1999, 9: 136-145.
10. Volek, J.S., Kraemer, W.J., Bush, J.A., et al. Creatine supplementation enhances muscular performance during high intensity resistance exercise. J Am Diet Assoc, 1997, 97: 765-770.
11. Moller, P., Bergstrom, J., Furst, P., and Hellstrom, K. Effects of aging on energy rich phosphagens in human skeletal muscle. Clin Sci, 1980, 58: 553-555.
12. Smith, S.A., Montain, S.J., Matott, R.P., et al. Creatine supplementation and age influence muscle metabolism during exercise. J Appl Physiol, 1998, 85 (4): 1349-1356.
13. Rawson, E.S., Clarkson, P.M., and Melanson, E.L. The effects of oral creatine supplementation on body mass, isometric strength, and isokinetic performance in older individuals. Med Sci Sports Exerc, 1998, 30: S140
14. Rawson, E.S., Wehnert, M.L., and Clarkson, P.M. Effects of 30 days of creatine ingestion in older men. Eur J Appl Physiol, 1999, 80: 139-144.
15. Crusch, Milibeck, P.D., Chad, K.E., et al. Creatine supplementation combined with resistance training in older men. Med Sci Sports & Exercise, 2001, 33: 12, 2111-2117.
16. Gordon A, et al. Creatine supplementation in chronic heart failure increases skeletal muscle creatine phosphate and muscle performance. Cardiovascular Research, 1995. Vol. 30:3,413-418.
17. Ferraro, S., Codella, C., Palumbo, F., et al. Hemodynamic effects of creatine phosphate in patients with congestive heart failure: a double-blind comparison trial versus placebo. Clin Cardiol, 1996, 19: (9), 699-703.
18. Tarnopolsky, M.A. Potential benefits of creatine monohydrate supplementation in the elderly. Curr Opin Clin Nutr Metab Care, 2000, 3: 6, 495-502.
19. Hespel, P.J.L., KU Leuven Research & Development, Belgium. Creatine compounds for prevention of aging effects and treatment of muscle atrophy. Eur Pat Appl. EP 1,002,532, 24 May, 2000.

No responses yet

May 08 2008

Turmeric Component Maintains Healthy Blood Sugar Levels in Animal Study

Published by under Turmeric

Curcumin, the compound in turmeric responsible for its yellowish color, improved insulin resistance and glucose tolerance in diabetic mice, according to the results of a new study.

The study authors investigated the effect of curcumin on insulin resistance and glucose tolerance in male diabetic mice and age-matched lean non-diabetic controls. Insulin resistance occurs when the body, after exposure to a constant onslaught of high blood sugar, needs to produce more and more insulin in order to feel insulin’s blood sugar stabilizing effects.

Both non-diabetic and diabetic mice were fed with or without curcumin for six weeks. At the study’s conclusion, there were a number of beneficial effects in the animals given the turmeric component. Curcumin significantly lowered blood glucose and levels of glycosylated haemoglobin HbA(1c), which researchers use as an indicator of blood glucose regulation. Curcumin also suppressed body weight loss in diabetic mice and reduced insulin resistance.

Furthermore, the researchers noted beneficial effects on the liver in the diabetic animals given curcumin. Activity of an enzyme that is important to the conversion of glucose into glycogen, which serves as the body”s main carbohydrate store, was higher in the diabetic mice given curcumin compared to the diabetic mice that did not receive the compound. The higher activity of the enzyme seen in the diabetic animals given curcumin is thought to inhibit the post-meal rise in glucose.

The turmeric-derived component also significantly lowered cholesterol and triglyceride concentrations and significantly reduced lipid peroxidation by virtue of its ability to raise antioxidant levels in the liver. In mice without diabetes, curcumin had no effect on blood glucose, plasma insulin, and glucose regulating enzyme activities.

The study authors wrote, “These results suggest that curcumin seemed to be a potential glucose-lowering agent and antioxidant in type 2 diabetic mice, but had no effect in non-diabetic mice.”

Reference:

Seo KI, Choi MS, Jung UJ, Kim HJ, Yeo J, Jeon SM, Lee MK. Effect of curcumin supplementation on blood glucose, plasma insulin, and glucose homeostasis related enzyme activities in diabetic db/db mice. Mol Nutr Food Res. 2008 Apr 8. Published online ahead of print.

No responses yet

Apr 21 2008

Key Nutrients Reverse Brain Aging Now Available in a Prescription formula

For years, the health of your brain cells was largely considered a one-shot deal: Your neurons had a single non-dividing lifespan — and once they were gone, there was no replacing them.

Making matters worse, any further loss of neurites and dendrites (the branches that form your brain’s massive communication network) could take what would be an otherwise normal loss of brain cells and turn it into a much more serious (and equally irreversible) condition — one marked by anything from minor physical and behavioral impairments to a state of complete senility.

Luckily, the scientific community has since done an about face on this particular matter.

More recent research has revealed that brain cells can replace themselves and regrow their communication networks, if given the right environment. In fact, just by boosting your intake of a few key nutrients, you can improve cognitive health — and even turn back the clock where cognitive decline has already started to settle in.

Among these nutrients, acetyl carnitine could be considered the most important. Laboratory studies have shown that this nutrient increases the revitalizing effects of nerve growth factor (NGF) on brain cells — helping to boost neurite outgrowth a full 100 times greater than NGF alone.1 And when taken in combination with acetyl carnitine arginate, the two act synergistically to boost the production of key neurotransmitters, like GABA and glutamate.2

These powerful effects are reflected in a number of human trials—all of which have shown that acetyl carnitine yields significant improvements in cognition.3

Uridine is also an important and little known ingredient for brain function—it provides the necessary components for cell membrane growth and memory-related neural signaling. In vitro analysis has revealed that human brain cells exposed to uridine experience increased neurite outgrowth and regeneration — results that carried over in vivo, when tested in aged rats.4-5

Similar applications can be seen with gotu kola, an Indian plant with a long history of use in Ayurvedic preparations for senility, epilepsy, and other nervous conditions. Studies performed in the last decade have only reinforced this reputation: Scientists have identified two of gotu kola’s unique compounds — asiaticosides and asiatic acid — as being particularly active, sparking repair of damaged neurons and higher brain functioning in both animal and in vitro studies.6

Complimentary Prescriptions, Neuron Growth Factors (NGF™)

A Rx formula that improves brain function by restoring the outgrowth of neurites on our brain cells. Neurites are the branch-like extensions (axons and dendrites) on brain cells where communication takes place. As we age, a reduction in this neurite network can occur, resulting in a corresponding loss of brain function.

Affected processes can include:

  • Alertness, focus and concentration
  • Cognitive (thinking) ability
  • Short term memory
    • Name, face recall
    • “What was I just saying…?”
    • “What did I come in here for…?”
    • “Where did I put my _____?
  • Ability to retain new information – “How do I work the remote again?”
  • Even hearing and spatial memory (sense of “where I am”) can be affected by neurite loss.

NGF is different from other kinds of brain products. Unlike other formulas NGF enhances brain function by actually improving the structure of brain cells through enhanced neurite outgrowth. Every aspect of brain function can benefit. NGF contains nutrients that have been shown to increase neurite outgrowth and help restore and enhance the structural basis of the brain’s neural communications network.

NGF contains acetyl l-carnitine (ALC) which has been shown to increase nerve growth factor activity as much as 100-fold. ALC increases the number of nerve growth factor receptor sites on brain cells, thereby enhancing the rate of neurite outgrowth. A related compound, acetyl carnitine arginate, works synergistically by mimicking the action of nerve growth factor itself.

Another ingredient, uridine, has been shown to regrow axons and dendrites during growth and development stages, as well as in older animals. Uridine has also been shown to improve cognitive function.

Gotu kola contains several active principals called asiaticosides. These improve cognition in older animals while stimulating axon-dendrite growth and out branching in key areas of the brain. Gotu kola has been used for centuries as a brain tonic in Indian and Chinese medicine and its use has been recorded for 2,000 years.

Gingko biloba has been shown to reduce the free radical oxidative stress produced by the presence of senile plaque in older brains. It is also able to improve undesirable structural changes to neurites caused by the presence of senile plaque. Gingko is a well-known promoter of blood circulation in the brain.

Recommended Dosage: See link below:

https://www.griffinmedical.com/shop/product.php?productid=342&cat=0&page=1

Griffin Medical Group (714) 549-6500

www.griffinmedical.com

References:

  1. Tagliatatela G, Angelucci L, Ramacci MT, et al. “Acetyl-L-carnitine enhances the response of PC12 cells to nerve growth factor.” Brain Res Dev Brain Res. 1991 Apr 24;59(2):221-30.
  2. Westlund KN, LU Y, Werrbach-Perez K, et al. “Effects of nerve growth factor and acetyl-L-carnitine arginyl amide on the human neuronal line HCN-1A. Int J Dev Neurosci. 1992 Oct;10(5):361-73.
  3. Montgomery SA, Thai LJ, Amrein R. “Meta-analysis of double-blind randomized controlled clinical trials of acetyl-L-carnitine versus placebo in the treatment of mild cognitive impairment and mild Alzheimer’s disease.” Int Clin Psychopharmacol. 2003 Mar;18(2): 61-71.
  4. Pooler Am, Guez DH, Benedictus R, et al. “Uridine enhances neurite outgrowth in nerve growth factor-differentiated PC12 [corrected].” Neuroscience. 2005; 134(1):207-14.
  5. Wang L, Pooler AM, Albrecht MA, et al. “Dietary uridine-5-monophosphate supplementation increases potassium-evoked dopamine release and promotes neurite outgrowth in aged rats. J Mol Neurosci. 2005;27(1):137-45.
  6. Soumyanth A, Zhong YP, Gold SA, et al. “Centella asiatica accelerates nerve regeneration upon oral administration and contains multiple fractions increasing neurite elongation in-vitro.” J Pharm Pharmacol. 2005 Sept;57(9):1221-9.

No responses yet

Next »

online pharmacy canada poker mtt statistics online pharmacy %?* remeron online Best price at buying viagra online [~); cheap viagra professional contact us or toll free.