Showing posts with label diabetes. Show all posts
Showing posts with label diabetes. Show all posts

Tuesday, June 18, 2013

Obesity Leads to Brain Inflammation, and Low Testosterone Makes It Worse


This is some seriously bad news for American men, 66% of whom are overweight or obese. One of the most debilitating side effects of obesity is that fats cells create estrogen - the more fat cells, and the bigger the fat cells, the more estrogen in the body. It gets worse, fat cells also support high levels of aromatase, an enzyme that converts testosterone to estrogen. More fat, less testosterone due to the aromatization of testosterone into estrogen .

High fat levels (through increases in estrogen due to aromatase conversion) reduce testosterone, which has its own downside: depression, loss of libido, muscle wasting, bone density loss, heart attacks and other cardiovascular issues, and higher risk of early death.

The evidence has been building for years that many neurodegenerative disorders, such as Alzheimer's Disease and other forms of dementia are linked to neuroinflammation (see this article). More recent evidence is showing that inflammation may play a crucial role in depression, schizophrenia, and bipolar disorder.

A 2012 article (Maintaining Brain Health by Monitoring Inflammatory Processes: a Mechanism to Promote Successful Aging) in Aging and Disease looked at how inflammation contributes to mental decline, as well as structural and metabolic dysfunctions. The article is freely available at the link above.
Abstract 
Maintaining brain health promotes successful aging. The main determinants of brain health are the preservation of cognitive function and remaining free from structural and metabolic abnormalities, including loss of neuronal synapses, atrophy, small vessel disease and focal amyloid deposits visible by neuroimaging. Promising studies indicate that these determinants are to some extent modifiable, even among adults seventy years and older. Converging animal and human evidence further suggests that inflammation is a shared mechanism, contributing to both cognitive decline and abnormalities in brain structure and metabolism. Thus, inflammation may provide a target for intervention. Specifically, circulating inflammatory markers have been associated with declines in cognitive function and worsening of brain structural and metabolic characteristics. Additionally, it has been proposed that older brains are characterized by a sensitization to neuroinflammatory responses, even in the absence of overt disease. This increased propensity to central inflammation may contribute to poor brain health and premature brain aging. Still unknown is whether and how peripheral inflammatory factors directly contribute to decline of brain health. Human research is limited by the challenges of directly measuring neuroinflammation in vivo. This review assesses the role that inflammation may play in the brain changes that often accompany aging, focusing on relationships between peripheral inflammatory markers and brain health among well-functioning, community-dwelling adults seventy years and older. We propose that monitoring and maintaining lower levels of systemic and central inflammation among older adults could help preserve brain health and support successful aging. Hence, we also identify plausible ways and novel experimental study designs of maintaining brain health late in age through interventions that target the immune system.
Full Citation:
Rosano, C, Marsland, AL, and Gianaros, PJ. (2012, Feb). Maintaining Brain Health by Monitoring Inflammatory Processes: a Mechanism to Promote Successful Aging. Aging and Disease; 3(1): 16–33. PMCID: PMC3320802


Two easy ways to control and reduce inflammation are an anti-inflammatory diet and regular exercise. Over at Integral Options Cafe, I posted information this morning on foods and supplements that reduce inflammation.

Here is the press release:

Obesity Leads to Brain Inflammation, and Low Testosterone Makes It Worse


June 17, 2013 — Low testosterone worsens the harmful effects of obesity in the nervous system, a new study in mice finds.

The results will be presented Monday at The Endocrine Society's 95th Annual Meeting in San Francisco.

"Low testosterone and obesity are common in aging men, and each is associated with type 2 diabetes and Alzheimer's disease," said the study's lead investigator, Anusha Jayaraman, PhD, of the University of Southern California in Los Angeles. "Our new findings demonstrate that obesity and low testosterone combine to not only increase the risk of diabetes but also damage the brain."

The study -- which was conducted in the laboratory of Christian J. Pike, PhD, Professor in the Davis School of Gerontology at USC and funded by the National Institutes of Health's National Institute on Aging -- consisted of three groups of male mice that received a high-fat diet (60 percent of calories were from fat) to induce obesity. Each group had eight mice and varied by testosterone status. One group had normal testosterone levels, and the second group underwent surgical removal of the testes so that the mice had low testosterone levels. The third group also underwent castration but then received testosterone treatment through a capsule implanted beneath the skin.

The high-fat diet, Jayaraman reported, resulted in obesity and evidence of diabetes -- abnormally high blood glucose (sugar) levels and poor glucose tolerance, which is the ability to clear glucose from the bloodstream. Compared with the group that had normal testosterone levels, the testosterone-deficient mice had more body fat, higher blood sugar levels and poorer glucose tolerance, she said.

After blood testing, brain tissues from the mice underwent analysis for changes. The brains of obese mice showed substantial inflammation and were less able to support nerve cell growth and survival, according to Jayaraman. These damaging effects of diet-induced obesity were significantly worse in mice with low testosterone, she said, adding that control groups of mice fed a normal diet did not show these changes.

"Our findings suggest that low testosterone and obesity interact to regulate inflammation of the nervous system, which may increase the risk of disorders such as type 2 diabetes and Alzheimer's disease," she said.

Because many of the negative outcomes of the high-fat diet were eased in the group of mice that received testosterone therapy, Jayaraman said that "testosterone treatment may be useful in reducing the harmful effects of obesity and low testosterone on the nervous system."

Saturday, October 20, 2012

Should Overweight Men Drink Caffeinated Coffee for Increased Testosterone and Reduced Estradiol?


I love when scientific research fails to confirm the working hypothesis but still produces a result that is significant in some way not originally intended. In this case, researchers were looking for a link between caffeinated or decaffeinated coffee consumption and any changes in sex hormone levels, specifically sex hormone-binding globulin (SHBG), in an attempt to understand how coffee consumption can reduce the occurrence of and severity of type II diabetes.

Study participants were regular coffee drinkers, nonsmokers, and overweight. Those is the coffee groups drank five 6-ounce cups a day with meals (either caffeinated or decaffeinated), while controls drank water.

After 8 weeks, they found that SHBG is unaffected by coffee intake, with or without caffeine. Interestingly, at the 4 week point, in men who consumed caffeinated coffee, there was a statistically significant increase in total testosterone and decrease in free and total estradiol. By the eighth week, however, there seemed to be no difference between the various treatment groups.

So, first of all, the subjects were overweight, which means they had high estrogen levels to begin with most likely. So if there is some polyphenol in coffee that helps the body clear estradiol and estrogen, then testosterone levels will automatically increase. But apparently this is true after four weeks but not eight.

Secondly, eight weeks is pretty short study to examine the effects of any substance on metabolism and hormones.

Finally, it appears the caffeine is the active ingredient. BUT, caffeine anhydrous (No Doze or Vivarin) is not the same as the complex caffeine in coffee or tea. I'd bet that a study pitting an equal amount of caffeine intake versus coffee would show that only the coffee is beneficial in this way.

Most likely, the results here point to only one mechanism of how coffee impacts diabetes anyway. I would still recommend coffee to my clients who can tolerate the caffeine.

The effects of caffeinated and decaffeinated coffee on sex hormone-binding globulin and endogenous sex hormone levels: a randomized controlled trial

Nicole M Wedick, Christos S Mantzoros, Eric L Ding, Aoife M Brennan, Bernard Rosner, Eric B Rimm, Frank B Hu andRob M van Dam

Nutrition Journal 2012, 11:86 doi:10.1186/1475-2891-11-86
Published: 19 October 2012
 

Abstract (provisional)


Background

Findings from observational studies suggest that sex hormone-binding globulin (SHBG) and endogenous sex hormones may be mediators of the putative relation between coffee consumption and lower risk of type 2 diabetes. The objective of this study was to evaluate the effects of caffeinated and decaffeinated coffee on SHBG and sex hormone levels.

Findings

After a two-week run-in phase with caffeine abstention, we conducted an 8-week parallel-arm randomized controlled trial. Healthy adults (n = 42) were recruited from the Boston community who were regular coffee consumers, nonsmokers, and overweight. Participants were randomized to five 6-ounce cups of caffeinated or decaffeinated instant coffee or water (control group) per day consumed with each meal, mid-morning, and mid-afternoon. The main outcome measures were SHBG and sex hormones [i.e., testosterone, estradiol, dehydroepiandrosterone sulfate].

No significant differences were found between treatment groups for any of the studied outcomes at week 8. At 4 weeks, decaffeinated coffee was associated with a borderline significant increase in SHBG in women, but not in men. At week 4, we also observed several differences in hormone concentrations between the treatment groups. Among men, consumption of caffeinated coffee increased total testosterone and decreased total and free estradiol. Among women, decaffeinated coffee decreased total and free testosterone and caffeinated coffee decreased total testosterone.
 

Conclusions

Our data do not indicate a consistent effect of caffeinated coffee consumption on SHBG in men or women, however results should be interpreted with caution given the small sample size. This is the first randomized trial investigating the effects of caffeinated and decaffeinated coffee on SHBG and sex hormones and our findings necessitate further examination in a larger intervention trial.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.