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Statins' Laundry List
According to a recent study not funded by a pharmaceutical company, in the journal Lancet, use of statins (Lipitor, zocor, etc) is associated with a small risk of developing diabetes. When looking at 90,000 subjects in this meta-analysis, it was found that there was a 9% increase in diabetes risk as compared to controls. This association was of greater significance with increasing age.
How does this affect you, statistically speaking?
Well, for every 255 patients treated with a statin medication for four years, there is the potential, according to the authors of this study, to produce one additional case of diabetes.
Add it to the Laundry List
This is yet another adverse effect added to statins’ already long list of side-effects. It means that physicians as well as patients have to be cognizant of this fact and monitor for signs and symptoms of glucose imbalance on a regular basis.
Remember that statin drugs are effective at reducing overall cardiovascular risk, so cardiologists will argue that the benefits of statins far outweigh the risks. From a conventional standpoint, it is, therefore, not recommended to change the existing indications for statin therapy in the setting of cardiovascular risk prevention.
Stay well and keep informed, Dr. K
Staying Ahead of the Curve on Parkinson’s Disease: Dementia and Green Tea
More recently, doctors are being urged
to treat dementia more aggressively inParkinson’s patients, as it would optimize quality of life for the patients andtheir caregivers. It is established that one third of patientswith Parkinson’s disease experience dementia. Cognitive impairments are the hallmark features, including decreasedattention span, executive functioning and memory deficits. Obtaining a legitimate diagnosis of dementiacan be quite tricky in that symptoms may widely fluctuate and therefore thediagnostic instruments that physicians use the diagnose Parkinson’s dementia maynot always give reliable results. Researchis conflicting at this point as to which is the best medical agent to use inthis population.
Thereare multiple safe nutritionally oriented treatments that patients may engage into help prevent early onset dementia as it related to Parkinson’s disease. First and foremost, optimization of diet iscritical. There is much research tosuggest that a diet that is high on the glycemic index scale can exacerbatedementia. Insulin resistance, associatedwith a diet that is chronically high on the glycemic index, has been associatedwith Alzheimer’s disease. The connectionhas been labeled type 3 diabetes by some. (See my published article under the References section of my websiteonthis topic).
Eatingorganic, MSG and pesticide free foods that can exacerbate both Parkinson’s aswell as dementia is important. Remember thatMSG can trigger glutamate receptors in Parkinson’s and non-Parkinson’s patientsalike. Followinga Mediterranean style diet that is high in unheated extra virgin olive oil,fish and poultry, nuts, vegetables, low glycemic index fruits, whole grainsthat are gluten free and unprocessed foods in key.
Just Do It
Addinga daily exercise component is imperative. Exercise can trigger dopamine levels to rise, help with coordination,drive down cortisol, improve insulin resistance, and help with mental acuity. These are all essential when hoping to helpprevent dementia and improve Parkinson’s symptoms. Exercise should include weight bearingexercise as well as core bodywork.
Theadrenal hormone DHEA has been shown to boost dopamine levels. There is also a significant amount ofresearch pointing to DHEA helping with improvement in memory in dementiapatients. DHEA is ever present in braintissue and helps to offset the negative effects of cortisol. It is, however, a precursor to many of theother hormones and needs to be used judiciously and under medicalsupervision.
Low grade chronicinflammation may be a precursor to neurodegenerative disease. An excellent anti-inflammatory program,including diet and supplements may help to quite the inflammation down.
Stay tuned for anarticle on coenzyme Q 10 and glutathione treatment in Parkinson's Disease.
Living Smarter, Living Longer,
Biggest Study Yet on Vitamin D and Colorectal Cancer Prevention
It seems like vitamin D is all we hear about lately. A flurry of well designed studies have been brought to light in the past decade. The largest study to date on vitamin D and cancer prevention confirmed several smaller studies which have suggested that higher blood levels of vitamin D are associated with lower risk for colorectal cancer.
Spanning 10 European countries and 520,000 subjects, vitamin D levels were measured and subjects were followed for 4 years after enrollment. 1248 of the subjects were then diagnosed with colorectal cancer. It was found that those with lower vitamin D 25 hydroxy concentrations (25-50 nmol/L) were associated with higher colorectal cancer risk and those with higher concentrations (75-100 nmol/L) had lower risk. Patients in the highest quintile had a 40% lower risk for CRC than those in the lowest quintile.
At this point I strongly believe that patients should be advised to take vitamin D in order to help prevent colorectal cancer. Such advice should be routine and definitely not considered "alternative."
CITATION(S):
Jenab M et al. Association between pre-diagnostic circulating vitamin D concentration and risk of colorectal cancer in European populations: A nested case-control study. BMJ 2010 Jan 21; 340:b5500.
Living Smarter, Living Longer
Dr. Kroner
Living Smarter, Living Longer
Dr. Kroner
Chocolate linked with Stroke Risk Reduction
No wonder everyone loves Canadians (and chocolate!). A literature review by Canadian researchers shows that higher chocolate consumption may be associated with a lower risk of stroke. This information will be presented in April 2010 at the American Academy of Neurology’s 62nd meeting.
Although the studies the researchers examined were small and the type of chocolate and its flavonoid content not clearly defined, this review warrants some attention. There has been prior research on chocolate consumption decreasing the risk of cardiovascular disease. Flavonoids are a category of antioxidants that have been associated with lower cardiovascular risk. Cocoa contains epicatechin, a type of flavonoid, which harbors a significant amount of antioxidant activity.
Antioxidants such as flavonoids protect the heart in a variety of ways:
- Prevents the oxidation of LDL – a process that occurs prior to plaque formation
- May mildly reduce blood pressure via the mechanism of arterial dilation and inproved blood flow
Can Mood Elevation Post Chocolate Intake Explain Decreased Risk?
The Journal of Internal Medicine in September 2009, published a study stating that survivors of heart attacks who ate chocolate at least two or three times a week reduced their risk of death by a factor of up to three times compared to survivors who did not eat chocolate. It is quite possible that this link is associated with chocolate consumption elevating serotonin levels. Elevated serotonin levels are associated with improved mood, which has been associated with better outcome after a cardiovascular event. Depression is a risk factor for cardiovascular disease. Can this very mood elevation prevent stroke as well? Are elevated brain serotonin levels at least part of the cause of chocolate contributing to stroke prevention? It is possible.
Do I Recommend a life of Chocolate Indulgence in Hopes of Stroke Prevention?
Hmmm. Remember to evaluate the risk vs. benefit ratio of this decision. Unless you are eating a small amount of pure dark chocolate that is not heavily sweetened, the amount of sugar in the average chocolate bar can put you at great risk for heart disease. The link between elevated blood sugar levels and heart disease is well established. Be careful to not fall into the trendy research trap. If we followed the research without judiciously weighing the risks, we would be swimming in wine, hot chocolate and caffeine. Sounds great for a day or two, until the consequences hit.
Living Smarter, Living Longer,
Dr. Kroner
HgA1C Better than Fasting Glucose at Predicting Risk for Heart Disease and Stroke
Many of you may have already been tested for pre-diabetes or diabetes using a marker called hemoglobin A1C (HgA1C). This test basically allows you to know how well your blood sugars have been controlled in the last three months. More recently, however, this test is becoming quite integral in predicting your risk of heart disease. According to the New England Journal of Medicine, levels above 6.0%, are better than fasting glucose for predicting long-term heart disease and stroke risk.
Scientists have known for years now that insulin resistance and diabetes have been tightly linked to cardiovascular disease, as the information is omnipresent. This is the one of the first studies comparing fasting glucose and HgA1C as they compare to assessing heart disease risk.
Why this May be
This may be so because fasting glucose is not as consistent a test. It will vary depending on what the patient ate the night before. It is not uncommon for patients to alter their diets slightly the night before the test in order to obtain a more favorable blood result. They may not have that glass of wine or extra helping of dessert. Therefore, unless they already have full blown out diabetes, their morning blood sugars may come back as normal.
A Hemoglobin A1c, however, is a more stable marker of one’s blood sugar control. The red blood cell has a life span of 120 days, during which glucose molecules react with hemoglobin. This forms a “glycated hemoglobin”, another term used for HgA1C. Those with poorer blood sugar control have a higher glycatred hemoglobin. A normal level is below 6.0%.
A standard American Diet will often cause spikes in blood sugar and therefore elevated the HgA1C. This, in turn, will increase the risk for multiple complications associated with both diabetes and insulin resistance; including coronary disease, vascular disease, heart attack, stroke, heart failure, kidney failure, blindness, erectile dysfunction, neuropathy (loss of sensation, especially in the feet), gangrene, and gastroparesis (slowed emptying of the stomach).
Now that a major journal is embracing the test for HgA1C, as opposed to a fasting glucose, as a measure of heart disease risk, I strongly believe that aside from routinely assessing its value, it is imperative to stay ahead of the curve and be proactive. Prevent heart disease and stroke by maintaining good control of your blood sugar. Keep the HgA1C low.
Living Smarter, Living Longer,
Dr. K
Question from Patient Suffering from Statin Side Effects
Dear Dr. Kroner,Thank you for this (Statin Side Effects) article. I was started on Pravachol 20 mg po q day approx. 6 weeks ago. After taking it for just 2 weeks, I stopped due to severe, activity-limiting muscle aches ( arms, thighs) and arthralgias (particularly in forearms, elbows, wrists and hands) accompanied by fatigue. These sx have persisted for 4 weeks now with a little improvement, but I'm still not able to do my usual moderate, regular exercise routine and feel exhausted. How long do these sx take to resolve? Are the arthralgias typical? Should I try CoQ10?
I'm an active, healthy 51yo female. My doctor doesn't think my sx are statin-related, wants me to try a lower dose or another statin, which I won't attempt until these sx resolve completely and I've investigated this further. Thank you for your thoughts. -
- Female (Anonymous) from Maryland
Hi,
Thank you for your note.
I am sorry to hear about your side effects. I see the side effects of myalgias and fatigue related to statin use regularly. On one occasion, I have witnessed arthralgia as a side effect. It may take up to 3 months for symptoms to resolve.
The most important thing to understand is whether or not you need the statin in the first place.
What is your risk of heart disease? Did your doctor recommend a coronary calcium score in order to figure out whether or not you have plaque in your arteries? One of the indications for statin use, according to the American Heart Association is coronary artery disease. I would also want to know what your other risk factors are: such as diabetes, smoking history, obesity, insulin resistance, sedentary lifestyle, family history of early onset coronary artery disease, etc.
I would want to perform blood tests that further risk stratify you: I would check a VAP cholesterol panel to assess your LDL particle size (the larger the LDL particle size, the less the chance that it will cause plaque formation), homocysteine, cardio-CRP, Lipoprotein (a), uric acid, HgA1C, fasting glucose, fibrinogen, fructosamine, etc. This will help to determine the degree to which you need the statin. I would definitely assess your baseline coenzyme Q 10 levels via a blood test. An average amount to take in the setting of statin use would be 100 - 200 mg of ubiquinol - the more bioactive form of coq10 daily with breakfast.
Hope this helps. Stay well.
Best,
Dr. Zina Kroner
Internist
The Second Brain: The Gut
This is not the “shock and awe” study of the year, but it elucidates an excellent medical phenomenon. A recent study in the American Journal of Gastroenterology showed that St. John’s Wort, an herb used to treat mild depression, was less effective than placebo at treating irritable bowel syndrome (IBS). Improvements in quality of life were similar in both placebo and the herb treated groups. Gastroenterologists have been treating IBS with anti-depressants for quite some time. I would like to bring to light the theory behind it, as this may have clinical implications beyond the use of medication.
The gut, often referred to as the second brain due to the powerful enteric nervous system that it houses, is tightly connected to serotonin, the feel good neurotransmitter. Dr. Michael D. Gershon, the chairman of the department of anatomy and cell biology at Columbia has brought this to light in his book entitled “The Second Brain.”
We have all felt a twinge in the stomach prior to a major exam or a public speaking event. It is quite common for my patients with a psychiatric disorder to have a concomitant gastrointestinal issue.
The Fight or Flight response and IBS
There are several reasons why stress or anxiety can cause irritable bowel syndrome. First, with any fight or flight response, cortisol, a stress hormone, is released. Cortisol fires up the sympathetic nervous system and makes the parasympathetic nervous system less efficient. It is the parasympathetic nervous system that we need in order to maintain bodily homeostasis, such as breathing, digestion,etc. Therefore, with a cortisol surge, digestion becomes ineffective and irritable bowel syndrome can kick in.
Serotonin and GI Function
Second, it is important to note that serotonin has a profound effect on gastrointestinal function, being that 95% of the body’s serotonin is cradled in the gut. At the start of digestion, it is the enterochromaffin cells that release serotonin into the gastrointestinal tract, which houses many serotonin receptors. The receptors then initiate a process via nerve cells that starts the flow of digestive enzymes.
Serotonin then relays messages up to the brain, letting it know what is happening. Therefore, certain foods may elicit a feeling of nausea, etc. Once serotonin is released in the gastrointestinal tract and the process of digestion is stimulated, normally, it is cleared out of the way by SERT, a serotonin transporter.
These transporters are found in the gut walls. Often, those with IBS, may not have an appropriate level of functioning SERTs, and they are therefore unable to clear out the serotonin cells. This can stimulate diarrhea. Once the serotonin receptors are supersaturated, the effect is constipation, thus the infamous Irritable Bowel Syndrome. Therefore, medications as well as supplements such as St. Johns Wort which manipulate the serotonin may potentially help IBS symptoms. It is no wonder that in this recent study, placebo was quite beneficial in IBS. This shows how much mind and body are connected. Focusing on stress management is key as well.
Delayed Food Allergy and Inflammation
A third contributor to IBS as it related to the enteric nervous system is allergens. Often, the barrier of the gut becomes damaged and certain allergens, etc, may enter the bloodstream, triggering the brain to send a message to the gut to increase the production of histamines and other inflammatory cells in order to try to get rid of the allergens. This inflammatory process may trigger the neurons in the enteric nervous system (in the gut) to become hyperactive and therefore contribute to diarrhea.
The challenge now is to optimize the efficiency of the gastrointestinal tract by preventing unnecessary cortisol surges so not to disrupt the sympathetic and parasympathetic nervous system harmony, to maintain a healthy serotonin and SERT level, and to prevent unnecessary allergens from entering the GI tract so not to trigger the inflammatory process involved in diarrhea. The gut really is the Second Brain!
Citation:
Saito YA et al. A randomized, double-blind, placebo-controlled trial of St John's wort for treating irritable bowel syndrome. Am J Gastroenterol 2010 Jan; 105:170.
Stay well,
Living Smarter, Living Longer...
Dr. K
Niacin Increases the Size of Your Cholesterol
Niacin has been more well known for its positive effects on HDL. Its effects on LDL have been more modest. Such modesty, however, deserves special attention in that it is indeed associated with an increase in LDL particle size and a shift from small LDL to the less atherogenic, large LDL subclasses. Therefore, we are looking at niacin from a standpoint of quality of LDL that it promotes, not just the quantity that it would reduce it by. This is a crucial point.
Note that a 2006 study in the American Journal of Cardiology showed that 3 months of ER niacin use in subjects w/ CAD increased large particle LDL by 82% and decreased small particle LDL by 12%.
Dr. K
My Patient's College Essay on Overcoming Alopecia Areata
The following is a college essay from a 17 year old patient of mine, Hallie, whose medical story is quite inspiring. She has given me permission to post it online.
"I was in the familiar position, sitting on a chair, hunched over, my long thick hair hanging in front of my face. My mother prodded and poked at the spot on my scalp right above the nape of my neck, looking at the red, scaly skin that was itchy, painful and extremely annoying. I was immediately alarmed when I heard my mother utter a gasp of shock. When she informed me that a round patch of my hair was missing, I went from feeling shocked to feeling a profound sadness. My mother never would have noticed this had she not been about to apply a cortisone cream to my already unfortunate dilemma of psoriasis. Psoriasis is a serious autoimmune disease that results in red, scaly patches on the skin. I was given several topical ointments to counteract the psoriasis, but some caused terrible side effects, and regrettably none were effective. By this point, I could no longer wear my hair in a ponytail for fear that my friends would spot my red scalp. We were both terrified and unsure of what this bald patch was. Was it a side-effect of the medication? Was it a symptom of psoriasis? We immediately made an appointment with the dermatologist to discover the answers to our questions.
As the doctor entered the room, my palms became sweaty and I trembled with fear. I had had an abnormal amount of skin problems in the past prior to having psoriasis, and I was worried that this could be the worst one of all. After examining my scalp, the doctor told me that I had a condition known as alopecia areata, an autoimmune disease which causes large patches of hair loss. The doctor seemed so calm regarding the situation, which angered me. By the frightened look on my mother’s face, I could tell that she was experiencing the same feelings as I was.
After discussing the diagnosis, he explained that the only treatment that might work was steroids. Rather than pills, however, I would be injected in my scalp wherever hair was missing. The doctor warned me that he could not promise that the hair would grow back, nor was there any treatment to cure the disease.
My mother and I immediately Googled “alopecia areata”, and the search results were terrifying. I was a 16 year old girl, a sophomore in High School, and going bald was one of the worst possible scenarios for me.
We were not satisfied with the inadequate medical solution the doctor prescribed for me, so we continued our investigation. We decided to get a second opinion from a well-known, respected doctor who practiced both conventional and alternative medicine.
Our first meeting with Dr. Kroner brought back another rush of fear of the unknown. But unlike the dermatologist, she was understanding, which enabled me to relax. She explained that psoriasis and alopecia areata are related because they are both autoimmune diseases. She predicted that I had sensitivities to certain foods that were preventing the absorption of necessary nutrients into my body. She administered extensive blood tests which confirmed her suspicions. The doctor prescribed a long list of vitamins and supplements in which I was deficient.
Dr. Kroner then educated me on the diet I would now strictly follow. I could no longer eat gluten (a protein found in wheat), casein (a protein found in dairy products), chocolate, sugar, soy, or oils other than olive oil. My eyes filled with tears as I thought about my favorite foods, ice cream and pizza, which at the time, I didn’t believe I could live without.
The following day I told my friends about my new diet. They were concerned and were curious as to why I had to deal with such a terrible predicament. I was too embarrassed to tell them that my hair was falling out so I told them I was experiencing stomach problems. It was hard to think about what would happen if my hair loss became noticeable. I was worried that I would be teased or pitied. I decided that at the moment, I should simply follow my diet and hope that my hair would grow back.
A few weeks later, a new health food store opened in my neighborhood. When I walked in, I saw that there was an entire gluten-free section! They had everything from cookies to pasta. I was overjoyed and felt suddenly at ease with my diet. Now I could snack on more than just nuts.
After a month, it was time for my next doctor visit. She told me that I should get the steroid injections from the dermatologist in order to speed up the growth process. We trusted her and returned to the dermatologist.
A few months later, my mother was checking my scalp as she regularly did when she noticed that not only had the psoriasis healed, but a few small hairs were beginning to grow back. We were extremely excited. However, other patches continued to fall out.
Throughout the duration of my disease, I continued working hard in school and participating in many extracurricular activities. Despite the dire situation, I managed to ignore it and continue to live my life. Instead of constantly worrying about the future of my disease, I maintained a positive attitude as well as my usual confidence. I was never one to get stressed, and so I put my disease out of my mind, while continuing my strict diet.
Hair continued to grow back to my delight. A year and a half later, I was told that there was no more hair loss. It was the most wonderful news! It was right after final exams of my junior year and the approaching end of my disease was a huge relief.
I believe that in addition to the diet, vitamins, supplements and steroid injections, I was able to overcome this disease because of my upbeat personality. I focused on my schoolwork and on achieving my goals and I avoided thinking about the negative aspects of life. I knew that letting depressing thoughts take over my life would not benefit me mentally or physically.
Fortunately, I was able to overcome this disease due to my perseverance and positive attitude. I could have let it consume my life, but instead I held my head up high and continued on ."
Hallie K., Long Island, New York
Photo of another alopecia areata patient:
Dr. K
Strategic Approach to Andropause, by Dr. Zina Kroner
I would like to bring to your attention an important article I wrote that features treatment strategies for andropause. (This article was originally published on www.drhoffman.com/page.cfm/531)
Menopause has been grabbing all the headlines lately, but half the world faces a comparable syndrome that is more insidious and less predictable. This disease entity is andropause.
Unlike menopause which usually occurs at a predictable time, men's testosterone levels decline at different ages and different rates, sometimes slowly, and sometimes precipitously. Testosterone production by the testes reaches adult levels by age 17 (300-1000 ng/dL). The testosterone level remains constant until the fifth decade at which point it declines at a rate of 1.2 percent per year. But in some men, testosterone can drop prematurely and precipitously.
In the Baltimore Longitudinal Study of Aging (2001), it was demonstrated that free testosterone decreased at a constant rate with age and this decline was not related to other causes. Another study demonstrated that poor health may accelerate the natural age-associated decline in testosterone concentrations. One interesting finding is that studies that measured testosterone in the morning were more likely to show a decline in testosterone when compared to studies that measured testosterone in the afternoon. The logic behind this is that older men have little variation in their levels of testosterone throughout the day, unlike young men, who have peaks in their testosterone levels in the morning and troughs in the evenings.
As one ages, there is an increase in fat cells, which in turn causes an elevation in an enzyme called aromatase. This enzyme transforms testosterone to estrogen in the body. Secondarily, estrogen can indirectly cause an increase in a protein called sex-hormone-binding-globulin (SHBG), which binds to free testosterone and prevents its action. This protein will ultimately cause a decrease in testosterone.
At this point you should be asking "Does this apply to me or to my spouse/partner?"
There are theories that demonstrate that a decline in testosterone can cause a decline in mental function. In a study published in the Journal Of Clinical Endocrinological Metabolism in 2002, 407 men were studied ages 50-91 and subsequently demonstrated that those classified as having a low testosterone had lower scores on memory and visuo-spacial performance. The results of several pilot studies have tied low testosterone levels to Alzheimer's disease, in which there is a build-up of a toxic peptide called beta-amyloid. These studies showed that the toxic effects of this peptide are reduced by testosterone. Interestingly, testosterone levels were lower in Alzheimer's patients as compared to controls. It is unknown if these low levels cause or are caused by Alzheimer's disease. According to Dr. Jonathan Wright (co-author of Maximize Your Vitality and Potency), low testosterone levels are associated with moodiness, feeling weak, passivity, and reduced interest in one's surroundings.
In addition to having an effect on cognitive function, studies have shown correlations between a declining testosterone level and a decline in sexual function as measured by frequency of orgasm or intercourse or by sexual satisfaction (Journal of Clinical Endoclinology 1983). Studies also show that muscle mass, muscle strength and bone mineral density decline with age.
The first step in diagnosing andropause starts with a thorough evaluation at your physician's office. First, your doctor will obtain a complete medical history from you and perform a series of blood tests to see if you have testosterone deficiency and what may be causing it. Before starting any treatment, however, it is imperative to rule out underlying prostate cancer, just as we would rule out breast cancer in a woman contemplating estrogen therapy. The following are some examples of causes of low testosterone and approaches to them.
First, as discussed, in obese patients, there is excess aromatase enzyme activity causing the testosterone to convert to estradiol causing estrogen overload and testosterone deficiency. Poor liver function is another entity that causes excess estrogen because the liver then cannot detoxify the small amounts of estrogen that even men have. In this case, total testosterone levels would be normal and estrogen levels would be high as much of the testosterone is being changed into estradiol, and the free or usable testosterone levels would be low. This often occurs with excess alcohol consumption.
If you fall into the above category, you should maintain an appropriately high level of aromatase inhibitors in your diet. The recommendation is zinc 80mg daily. A supplement call chrysin, a flavonoid, together with piperine for enhance absorption into the bloodstream, functions as a mild aromatase inhibitor as well. There is a more potent aromatase- inhibiting drug called Arimidex (anastrozole), which can only be prescribed by your doctor. Arimidex is prescribed to estrogen receptor positive breast cancer patients to prevent hormones in the body from aromatizing into estrogen. It has not yet been FDA approved for other indications.
A diet that does not adversely affect liver function should be adhered to. This will of course include an alcohol-free diet, since even small amounts of alcohol are shown to augment estrogen in both men and women. Special attention should be paid to medications affecting the liver and should be reviewed with your doctor in detail. As estrogen excess may be a problem in the setting of liver dysfunction, a substance called indole-3-carbinol (or diindole methane or DIM)) found in special supplements or cruciferous vegetables can help to neutralize the excess estrogen. Most importantly, it is essential that you lose weight as it is the excess aromatase enzyme that is produced by the fat cells that convert the testosterone into the estrogen.
Second, an excess of sex-hormone-binding-globulin can bind much of the free- testosterone and therefore inactivates it. In this case, one will have low free testosterone, normal or even high total testosterone and normal estradiol levels. In addition to following the protocol that inhibits aromatase activity, take saw palmetto which can block the estrogen receptor sites in the prostate cells and therefore reduce the effects of excess estrogen. Saw palmetto also blocks the conversion of testosterone into a hormone, DHT, which has been directly linked to the development of prostate disease.
Methanolic extract of nettle can also inhibit SHBG. It binds to SHBG and therefore blocks its testosterone binding effects, thus allowing more testosterone to be in its natural free state. This root has also been used for benign prostatic hyperplasia. It inhibits the binding of dihydrotestosterone ( DHT), a prostate growth stimulator, to the prostate.
A third cause of low testosterone is failure of the pituitary gland to produce a hormone called leutenizing hormone (LH). One of the functions of LH is to stimulate testosterone production by the testes. In this case, the levels of total testosterone would be low as there is a problem with production.
Fourth, if the testes themselves lose their ability to produce testosetrone, there would be an elevated LH, which would act as a stimulant to produce testosterone. Total testosterone would be low. Patients like these are candidates for testosterone replacement.
Lastly, DHEA, a precursor hormone to testosterone and estrogen, may be low and worsen the consequences of borderline testosterone. The solution here is to supplement DHEA under a doctor's supervision.
Physicians have prescribed testosterone administered via creams, tablets, patches, lozenges and injections. Such preparations can lead to normalization of testosterone and improvements in muscle strength, libido, mood and bone density. They may also be associated with side effects, so care must be taken to use the right form of replacement and dosage. There is no "one size fits all" approach.
After initiating testosterone, during the first few months, some men may note effects seen in normal puberty, such as acne and gynecomastia. In men over the age of 50, worsening of prostate symptoms may occur, although sometimes they improve. If, however, the testosterone is not taken in excess and used to maintain a normal serum testosterone, there is no reason to believe that these men are more likely to develop these conditions than men who produce their own natural testosterone. Nevertheless, a PSA and a digital rectal exam and close monitoring of hormone levels must be adhered to.
Living Smarter, Living Longer
Dr. K
