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@pmgamer18 6832 wrote:
Thank you Definitive Mind for the Birthday Email.
Today I am 69 yrs. old Thank you GOD for one more year.Happy Birthday Phil!!!
Deficient maternal vitamin D associated with low infant birth weight
December 21, 2012. The January 2013 issue of the Journal of Clinical Endocrinology & Metabolism reports the finding of researchers at the University of Pittsburgh of a relationship between reduced vitamin D levels in pregnant women and a higher risk of delivering a low birth weight infant. Babies who are born with a low birth weight have a greater chance of dying during their first month of life and experience more chronic diseases later, including type 2 diabetes and cardiovascular disease.
Alison Gernand, PhD, MPH, RD of the University of Pittsburgh’s School of Public Health and colleagues measured 25-hydroxyvitamin D levels among 2,146 pregnant women who participated in the Collaborative Perinatal Project between 1959 to 1965. Women whose vitamin D levels were 37.5 nanomoles per liter (nmol/L) or greater gave birth to infants whose birth weight averaged 46 grams higher than children born to mothers whose vitamin D levels were lower than 37.5 nmol/L. In addition, infants born to mothers with higher vitamin D levels had larger average head circumferences than those born to women with lower levels.
“A mother’s vitamin D level early in pregnancy may impact the growth of her baby later in pregnancy,” stated Dr Gernand, who is a post-doctoral associate in the School’s Department of Epidemiology. “Also, if the mother was deficient in vitamin D during the first trimester, her baby had twice the risk of suffering from growth restriction in utero.”
“This is one of the largest studies to examine a mother’s vitamin D levels and their relationship with birth weights,” added senior author Lisa M. Bodnar, PhD, MPH, RD. “It shows that clinical trials to determine if you can improve birth weights by giving women of reproductive age vitamin D supplements may be warranted.”
Vitamin D supplementation reduces respiratory infection
December 17, 2012. Researchers from Sweden’s Karolinska Institut report on December 13, 2012 in the journal BMJ Open that supplementation with vitamin D significantly reduced respiratory tract infections among men and women at risk of contracting them.
In the current study, 124 men and women with an antibody deficiency or history of more than four bacterial respiratory tract infections per year were given 4,000 international units (IU) vitamin D per day or a placebo. The subjects were asked to keep a daily record of symptoms arising from the respiratory tract, ears and sinuses; antibiotic treatment, and other factors. After a year of treatment, composite infectious scores were calculated for each participant.
Subjects who received vitamin D had approximately 25 percent fewer respiratory tract infections and nearly half the antibiotic use than those who received the placebo. The findings are in contrast with those recently described in the Journal of the American Medical Association (JAMA) in which vitamin D failed to show a protective effect against viral respiratory tract infection incidence or severity in a New Zealand population. However, the JAMA study involved healthy individuals whose vitamin D levels at the beginning of the study were normal, and the vitamin was administered in large doses on fewer occasions, which is believed to be less effective than daily administration. “The most important difference is probably due to the fact that our participants had much lower initial levels of vitamin D than those in the New Zealand study,” commented study coauthor Dr Anna-Carin Norlin of the Karolinska Institutet’s Department of Laboratory Medicine.
Lead author Peter Bergman noted that “Our research can have important implications for patients with recurrent infections or a compromised immune defense, such as a lack of antibodies, and can also help to prevent the emerging resistance to antibiotics that come from overuse.”
Insufficient vitamin D could explain alcoholism-related muscle condition
December 19, 2012. In a review published online on December 14, 2012 in Alcoholism: Clinical & Experimental Research, Jan W. Wijnia of Slingedael Korsakoff Center in the Netherlands and colleagues suggest that insufficient vitamin D levels could account for the high prevalence of myopathy in men and women suffering from chronic alcoholism. Vitamin D deficiency is a known cause of myopathy, and alcoholism has been associated with reduced levels of the vitamin. “Myopathy simply means ‘muscle disease,'” Dr Wijnia explained. “Muscle weakness is by far the most frequent symptom of alcoholic myopathy, causing difficulties in rising from a chair or in climbing a staircase. In alcoholic myopathy, improvement of muscle weakness usually occurs six to nine months following alcohol abstinence.”
For their review, the researchers selected 93 articles concerning myopathy related to reduced levels of vitamin D and myopathy associated with alcoholism. “Our review links possible interdependent deficiencies of vitamin D, phosphate, and magnesium with muscle weakness in chronic alcoholism,” Dr Wijnia stated. “Previous studies had suggested that changes in alcoholic muscle disease were not due to dietary deficiencies, but our review is one of the few to examine the effects of severe vitamin D deficiency in alcoholic myopathy.”
“The causes of vitamin D deficiencies in alcoholics may include liver dysfunction, lack of sun exposure, malabsorption, and inadequate dietary intake,” he added.
“We recommend future research focusing on possible beneficial effects of vitamin D supplementation and on optimal dosages,” he continued. “It is possible that vitamin D supplementation may assist in prevention and treatment of alcohol-related chronic myopathy, thus, assessment of vitamin D status may help clinicians to early diagnose severe vitamin D deficiency and hence offer appropriate treatment. Further research is needed to determine if this can improve muscle function if alcohol consumption ceases, and what dosages of vitamin D may be optimal.”
Vitamin D anticancer mechanism revealed
December 31, 2012. The November 13, 2012 issue of the Proceedings of the National Academy of Sciences reported the discovery of researchers at McGill University in Montreal of a mechanism for vitamin D against cancer. Numerous studies have uncovered associations between higher vitamin D intake or serum levels and a lower risk of cancer; however, the protective mechanisms of the vitamin have not been fully explored.
Professors John White and David Goltzman of McGill’s Department of Medicine and their colleagues discovered that the active form of the vitamin, known as 1,25‑dihydroxyvitamin D, inhibits the production and function of cMYC, a transcription factor involved in cell division that is active in at least 50 percent of cancers. In an experiment conducted by the McGill team, 1, 25‑dihydroxyvitamin D was found to inhibit the transcription of genes regulated by cMYC. And in a study in which vitamin D was applied to the skin of mice, cMYC was suppressed and an antagonist of the protein known as MXD1 increased.
“For years, my lab has been dedicated to studying the molecular mechanisms of vitamin D in human cancer cells, particularly its role in stopping their proliferation,” Dr White remarked. “We discovered that vitamin D controls both the rate of production and the degradation of cMYC. More importantly, we found that vitamin D strongly stimulates the production of a natural antagonist of cMYC called MXD1, essentially shutting down cMYC function”.
“Taken together, our results show that vitamin D puts the brakes on cMYC function, suggesting that it may slow the progression of cells from premalignant to malignant states and keep their proliferation in check,” he concluded. “We hope that our research will encourage people to maintain adequate vitamin D supplementation and will stimulate the development of large, well‑controlled cancer chemoprevention trials to test the effects of adequate supplementation.”
Vitamin D needed by women to maintain cognitive health
December 3, 2012. The October, 2012 issue of the Journals of Gerontology Series A: Biological Sciences and Medical Sciences published the outcome of a study conducted by Yelena Slinin, MD, MS, of Minneapolis’ Veterans Administration Medical Center which uncovered a protective effect for higher vitamin D levels against the development of cognitive decline in women.
The study included 6,257 women enrolled in the Study of Osteoporotic Fractures. Serum 25-hydroxyvitamin D was measured upon enrollment and tests of cognitive function were administered at the beginning of the study and at follow-up after four years. Women with low vitamin D levels of less than 10 nanograms per milliliter (ng/mL) had a 60 percent greater risk of cognitive impairment at the beginning of the study and a 58 percent greater risk of becoming cognitively impaired over follow-up in comparison with those whose levels were at least 30 ng/mL.
In another study published in the November, 2012 issue of the same journal, Cedric Annweiler, MD, PhD, of Angers University Hospital in France and his associates report an association between reduced vitamin D intake and a greater risk of developing Alzheimer’s disease. The study included 498 older women enrolled in the EPIDemiology of OSteoporosis Toulouse cohort study. Dietary questionnaires administered at the beginning of the study were analyzed for the intake of vitamin D from food sources. Over a seven year period, 70 participants developed Alzheimer’s disease. In comparison with those who did not develop dementia or developed other types of dementia, women who developed Alzheimer’s disease consumed less vitamin D. When participants were grouped according to vitamin D intake, those in the top one-fifth were found to have a 77 percent lower risk of Alzheimer’s compared to the lowest fifth.
These studies, and others, reinforce the importance of vitamin D in the maintenance of cognitive health over the course of a lifetime.
Since when did we learn that HRT causes cancer?
I am not talking about progestin for menopause, but bioidentical HRT.
@DrMariano 6694 wrote:
The primary purpose of a binding protein such as SHBG is to prolong the life of testosterone in the body. Otherwise, with a half-life of 10-100 minutes – testosterone would be almost totally eliminated from the body within 50 minutes to 8.3 hours without constant production or frequent application of testosterone.
The quickest way to increase SHBG is to treat a person with T3 (Cytomel) or to a lesser extent Armour Thyroid, when optimizing thyroid hormone signaling. This increases SHBG production from the liver. Optimizing thyroid signaling first is important to set the stage for subsequent testosterone treatment. Doing so helps correct low SHBG.
Low SHBG is one of many reasons testosterone levels are so low in diabetes type 2. When SHBG is low due to insulin resistance/diabetes type 2 and high insulin level, treatment with testosterone helps reduce insulin resistance. Over several months time, SHBG self-corrects as other metabolic improvements with testosterone treatment occur such as loss of belly fat. Of course, in the presence of diabetes type 2, one of the first things to do is to optimize thyroid hormone and treat the insulin resistance with medications such as Metformin or Actos. This would help improve SHBG and would set the stage for testosterone treatment, minimizing problems that can occur with testosterone treatment – such as anxiety, irritability, fatigue, excessive estrogen, etc.
Low SHBG also occurs in inflammatory diseases (such as rheumatoid arthritis, etc.) – where Interleukin 1 beta reduces SHBG production. I generally assess for the presence of immune system problems since they are often at the root of mood disorders. Reducing pro-inflammatory signaling would help correct their role in reducing SHBG.
SHBG is important but usually it is self-corrected by addressing more important problems – such as hypothyroidism, diabetes, chronic inflammatory illness – prior to testosterone replacement.
When it does become a significant problem is when it is too high – such as with high dose T3 treatment in cases of peripheral thyroid resistance. When SHBG is high, a normal 100 mg a week dose of testosterone cypionate can achieve blood levels past 1500 ng/mL. A concern at that level when coupled with high SHBG is that the lower free testosterone levels may become a significant factor in reducing the effects of testosterone. SHBG bound to testosterone does have signaling function on its own – what it does is unclear – but it is interesting to speculate that if the testosterone-bound SHBG signal is too high, perhaps it may inhibit libido.
Dr. M,
You often mention, including in your response above, that you evaluate for inflammation. What tests do you prefer to gauge a patients level of inflammation?
thank you.
Dr Mariano,
Have you noticed any of the amino acids that are dopamine precursors to be useful in helping libido?
Have you noticed high Prolactin to be a libido killer? if so, at what level? and what has been your experience in treating?
thank you as always.
Am I reading correctly that your Total Testosterone level is far below the bottom of the reference range?
If so, getting to upper quartile may go a long way to helping you feel better.
@DrMariano 4759 wrote:
Excessive reduction of inflammatory signaling causes insomnia in some people.
One cannot arbitrarily reduce inflammation. Just like most things, there needs to be a “normal” or appropriate amount of inflammation for function. For example, aside from impairing one’s ability to fight infection, excessive reduction in inflammatory signaling impairs the brain’s ability to reconfigure neural networks into new patterns which we call memory.
The traditional Eskimo diet has about 2400 mg of Omega-3 a day. I use that as a starting point.
Interesting, am I to gather from this that being in a pro-inflammatory state keeps one from getting sick? I haven’t had a bad cold or missed a day of work EVER at my job and I’m in my 17th year there.
As stated, I have become convinced I have excessive norepiniphrine. I have poor libido, ED and PE. I can orgasm with ease, mutiple times in hours, but always with very poor erections and lack of feeling. Just kinda happens.
To complete my iron labs:
Iron 52 (45-170)
TIBC 287 (250-450)
Transferrin Saturation 18 (20-55)
UIBC 235 (110-370)
Ferritin 96 (20-250)Thank you for your detailed response.
While I am not a doctor, I do have the advantage of living with my body every moment of my life. By reading information from yourself and Dr. Crisler over the past years, I pay very close attention to how I feel and comapre ot what I have learned.
I have become increasingly convinced, I have an overactive Sympathetic Nervous System, cause of which I am not sure. I often see you post abpu the effects of too much norepiniphrine and how it can inhibit erections and libido. Need it, but not too much.
Even though my last Testosterone blood test showed only 360, a 24h urine test done at the same time ,showed DHT above range. I believe I read once that Dr. J stated that sometimes, it seems androgens can all be driven to DHT and can “burn up the circuits” so so to speak.
How do you feel about such a scenario?
What causes excessive DHT? How to combat without risking Finasteride?
Progesterone counters?
I have used a Mindful practice to help calm myself down, but this doesnt seem to be enough.
thank you again.
I enjoy Jon Kabat-Zinn and his talks, books, practices. “Wherever You Go, There You Are” is a great book as are his CD programs on Mindfulness. He has done plenty of research that shows the affects of a mindful meditation practice on the the brain.
Here is a talk he gave at Google with a short mediation sequence and Q&A. It is something that I got more out of each time I watched and listened. Enjoy.
