Tuesday, April 22, 2014

Best supplements for men's health and strength

I had a request to write a post on the top supplements for men's health and strength. Many or most of these will be beneficial to just about everyone, young or old, men and women. But for men, especially those of us who lift weights, we'll want to emphasize effects on testosterone levels, muscle anabolism, and strength.

1. Whey protein. Whey protein can benefit just about everyone; for instance, I've got my elderly mother taking a whey shake daily. Whey prevents oxidative stress due to its high cysteine content which helps replenish glutathione, the body's critical antioxidant. Whey's high content of branched-chain amino acids promotes muscle anabolism as well as actual increased lifespan. Whey is about 50% essential amino acids, about the highest of any protein, and EAAs alone are responsible for increased anabolism. Increased anabolism means that it helps strength athletes as well as helps prevent sarcopenia in the elderly. Dose: 20 g/d for general health, possibly more for anabolism. I personally take this before my workouts, so it provides a high level of amino acids in the blood and to the muscle while the muscle can most use it. I also like the whey they sell at NutraBio.com, as it's cold-processed and non-denatured, which leaves bioactive peptides intact and is the most healthful kind.

2. Creatine. This is now being touted for everything from treating Alzheimer's to increasing longevity. For men who lift, they'll recognize it as one of the most thoroughly studied and effective ergogenics around. Supposed downsides, such as effect on kidney function, appear to be all but nonexistent. Dose: ~5 g/d.

3. Fish oil / omega-3 fats. These have beneficial effects on inflammation and with it, heart disease and cancer. For men's strength in particular, they're anabolic. Omega-6/3 ratios are wildly out of whack in modern society. If you eat a good diet devoid of industrialized foods, you may need probably a minimal dose. (And if you do eat industrial foods, stop.) My dose: one tsp. daily. In chronic illness, you may need more. (Avoid fish oil capsules, and refrigerate cod liver oil.)

4. Magnesium. This is the one mineral that most people are likely to be deficient in, with up to 60% of Americans deficient. Required for over 300 enzymatic reactions. Boosts T levels. Fights depression. Promotes longevity. Magnesium oxide (common drugstore kind) is very poorly absorbed; get magnesium citrate. Dose: 200 mg/d, more if you are deficient and need to play catch-up, or are not in greatest of health. Best taken at bedtime, as it can promote relaxation and better sleep.

5. Vitamin D. Much has been said in recent years about this. Sun avoidance and working indoors as well as poor diet means many are deficient. It is possible to take too much, but 2,000 IU a day would be a good place to start, more if body weight is higher. For details on dosing and related matters, I recommend reading the folks at The Vitamin D Council.

6. Zinc. Zinc boosts T levels and does all kinds of other things, notably increasing immunity. Many people are deficient, but if you eat whole foods featuring plenty of meat, you should be OK. I take 50 mg once a week for insurance. If you determine that you are deficient, more can be taken, but not more than 20 mg/d.

7. Resveratrol. Pretty much the proven longevity extender. Boosts mitochondrial function and number (which is intrinsic to its lifespan increasing activity), which will increase energy levels. Bonus: it inhibits aromatase too. I take 250 mg/d but not on workout days, since it inhibits mTOR. (Note: a putative link between resveratrol and effect on workouts is purely my speculation; R does effect mTOR, but to my knowledge there's no research on an anabolism effect, and my guess is that it's too weak an effect to matter.)

8. Aromatase inhibitor. This one strictly for the men. Especially as men get older, their aromatase enzyme activity increases, meaning that more T gets converted to estrogens, especially estradiol, which is the most potent estrogen. In turn, estrogens are the most important negative feedback inhibitor of LH, which controls T production. Ergo, inhibit aromatase, decrease estradiol, LH levels increase, T increases. This works on both normal T young men as well as low T older men, increasing T levels by ~50% or more, depending on dose. Downside: you need a prescription, but OTOH I believe that most doctors will be more willing to prescribe this than to prescribe T replacement therapy. (In their defense, they're scrutinized pretty heavily.) In any case, anastrozole, the main AI, is now generic and cheap and only low doses are needed.

9. Vitamin C. There's been a lot of controversy as to whether C impairs adaptations to exercise, and I remain agnostic on the issue. But I don't take this daily, and not on workout days. But, it appears that most people could use more than they're getting. Suggested dose: 1 g a few times weekly.

10. N-acetylcysteine. This supplement helps replenish glutathione (as whey does), and alleviates oxidative stress. The thing is, it's turning out that transient oxidative stress is not at all bad, and is necessary for many longevity and exercise related effects. If one is ill, I recommend this; but if one is in general good health and not elderly, whey protein has similar benefits and I would probably stick to that. NAC has been found quite beneficial for many mental illnesses, such as depression, so if one suffers from that, look into it. I took it when I had chronic fatigue, but no longer do. NAC is OTC, cheap, and safe.

There are a few more; e.g. vitamin K is hard to get in the diet, so I supplement a few times a week. I was going to add links to the above, but since I've covered virtually all of it on this blog, I'll ask that you just search around or use the topic headings listed at the side of the blog. Questions/suggestions welcome.

Monday, April 21, 2014

Coronary heart disease to become a thing of the past

The following chart is from the blog of Dr. David Grimes.



Dr. Grimes writes:
At the peak of the epidemic in 1970 there were 520 deaths per 100,000 per year in England and Wales, 700 in the USA, and an astounding 960 in men in the West of Scotland, the world's highest incidence. Thereafter there was an abrupt and apparently spontaneous decline, by 83% during the next 20 years to 1990. This is an important observation as during this time there was no widespread effective medical intervention.

The decline continues. At present the death rate is about 20 per 100,000 per year and the decline appears to continue. We appear to have experienced a natural epidemic and it is now almost over. The cause of it has not been obvious, but when we realise that CHD has been an epidemic we can start to think objectively about what might have caused it.
I grew up in that era when men had to be concerned about their death or disability from a heart attack. It looks as if that era may be coming to a close. But what caused the rise in coronary heart disease, and what accounts for its fall? Seems a bit mysterious. Smoking seems a likely candidate, but the rise and decline in cigarette smoking doesn't exactly track the rates of heart disease, the decline of which seems to have begun before smoking declined.

Sunday, April 20, 2014

Can drinking water promote weight loss?

Oddly enough, drinking water increases the metabolic rate substantially: Water-induced thermogenesis.
Drinking lots of water is commonly espoused in weight loss regimens and is regarded as healthy; however, few systematic studies address this notion. In 14 healthy, normal-weight subjects (seven men and seven women), we assessed the effect of drinking 500 ml of water on energy expenditure and substrate oxidation rates by using whole-room indirect calorimetry. The effect of water drinking on adipose tissue metabolism was assessed with the microdialysis technique. Drinking 500 ml of water increased metabolic rate by 30%. The increase occurred within 10 min and reached a maximum after 30-40 min. The total thermogenic response was about 100 kJ. About 40% of the thermogenic effect originated from warming the water from 22 to 37 C. In men, lipids mainly fueled the increase in metabolic rate. In contrast, in women carbohydrates were mainly used as the energy source. The increase in energy expenditure with water was diminished with systemic beta-adrenoreceptor blockade. Thus, drinking 2 liters of water per day would augment energy expenditure by approximately 400 kJ. Therefore, the thermogenic effect of water should be considered when estimating energy expenditure, particularly during weight loss programs.
The mechanism by which water does this is somewhat mysterious. A later paper by the same group, Water Drinking Induces Thermogenesis through Osmosensitive Mechanisms, found that saline solution had no effect.
Only 500 ml water increased energy expenditure by 24% over the course of 60 min after ingestion, whereas isoosmotic saline and 50 ml water had no effect. Heart rate and blood pressure did not change in these young, healthy subjects.
Conclusions: Our data exclude volume-related effects or gastric distension as the mediator of the thermogenic response to water drinking. Instead, we hypothesize the existence of a portal osmoreceptor, most likely an ion channel.
I am a little skeptical of the authors' claim that this might help weight loss, since other homeostatic mechanisms would come into play, but sure enough, a paper looked at that, and found that water drinking is associated with weight loss: Drinking Water Is Associated With Weight Loss in Overweight Dieting Women Independent of Diet and Activity.

Learn something new every day.

On the other hand, another study, Water-Induced Thermogenesis Reconsidered: The Effects of Osmolality and Water Temperature on Energy Expenditure after Drinking, could find no effect of water drinking on metabolism. Oh, well.

Friday, April 18, 2014

High-protein diet improves reaction times

Effect of a high protein meat diet on muscle and cognitive functions: A randomised controlled dietary intervention trial in healthy men
Background

Recommendations to use other criteria than N-balance for defining protein requirements have been proposed. However, little evidence to support other measures such as physiological functions is available.

Objective

To investigate the effects of a usual (UP) versus a high protein (HP) diet on muscle function, cognitive function, quality of life and biochemical regulators of protein metabolism.

Design

A randomised intervention study was conducted with 23 healthy males (aged 19–31 yrs). All subjects consumed a Usual Protein (UP) diet (1.5 g protein/kg BW) for a 1-wk run-in period before the intervention period where they were assigned to either a UP or a High Protein (HP) diet (3.0 g protein/kg BW) for 3-wks with controlled intake of food and beverages. Blood and urine samples were taken along with measurements of physiological functions at baseline and at the end of the intervention period.

Results

The HP group improved their reaction time significantly compared with the UP group. Branched chain amino acids and phenylalanine in plasma were significantly increased following the HP diet, which may explain the improved reaction time.

Conclusion

Healthy young males fed a HP diet improved reaction time. No adverse effects of the HP diet were observed.
The fact that this occurred in healthy young men means that it's not an effect of overcoming age, illness, or malnutrition, but points to the possibility that most people are not eating enough protein.

Wednesday, April 16, 2014

Vitamin D and whether you'll leave the hospital dead or alive

Association of low serum 25-hydroxyvitamin D levels and mortality in the critically ill.
We hypothesized that deficiency in 25-hydroxyvitamin D before hospital admission would be associated with all-cause mortality in the critically ill....

MEASUREMENTS AND MAIN RESULTS:
...Preadmission 25-hydroxyvitamin D deficiency is predictive for short-term and long-term mortality. At 30 days following intensive care unit admission, patients with 25-hydroxyvitamin D deficiency have an odds ratio for mortality of 1.69 (95% confidence interval of 1.28-2.23, p < .0001) relative to patients with 25-hydroxyvitamin D sufficiency. 25-Hydroxyvitamin D deficiency remains a significant predictor of mortality at 30 days following intensive care unit admission following multivariable adjustment (adjusted odds ratio of 1.69, 95% confidence interval of 1.26-2.26, p < .0001). At 30 days following intensive care unit admission, patients with 25-hydroxyvitamin D insufficiency have an odds ratio of 1.32 (95% confidence interval of 1.02-1.72, p = .036) and an adjusted odds ratio of 1.36 (95% confidence interval of 1.03-1.79, p = .029) relative to patients with 25-hydroxyvitamin D sufficiency. Results were similar at 90 and 365 days following intensive care unit admission and for in-hospital mortality. In a subgroup analysis of patients who had blood cultures drawn (n = 1160), 25-hydroxyvitamin D deficiency was associated with increased risk of blood culture positivity. Patients with 25-hydroxyvitamin D insufficiency have an odds ratio for blood culture positivity of 1.64 (95% confidence interval of 1.05-2.55, p = .03) relative to patients with 25-hydroxyvitamin D sufficiency, which remains significant following multivariable adjustment (odds ratio of 1.58, 95% confidence interval of 1.01-2.49, p = .048). CONCLUSION: Deficiency of 25-hydroxyvitamin D before hospital admission is a significant predictor of short- and long-term all-cause patient mortality and blood culture positivity in a critically ill patient population.
No one knows when they're going to end up critically ill and/or in the hospital. But if you want to live through the experience and come out the other end alive, make sure you're vitamin D sufficient.

The blood culture positivity is interesting. As is well known, hospital-acquired infections are a major problem, including blood-borne infections; the latter are extremely serious and have a high fatality rate. I can think of no other reason for vitamin D levels to be associated with blood infections other than causality: vitamin D deficiency causes a defect in immunity.

I'm not sure why, given results like these, that hospitals wouldn't ensure that all of their critically ill patients are vitamin D sufficient.

Tuesday, April 15, 2014

Why modest nutrient deficiencies can lead to disease

It's sometimes said that truly healthy people need no supplements, but personally I doubt that, except in perhaps a small fraction of cases. For one thing, illnesses can be hidden, so that we don't who the truly healthy really are. Another is that it is difficult in our modern food system to naturally consume all the nutrients needed in the right quantities. For instance, it seems most people could use more omega-3 fatty acids and magnesium and vitamin D than they get from their environment. (Just to cite the three that came to mind the quickest.)

Renowned biochemist Bruce Ames, still going strong, has put forward a triage theory of nutrition. Basically, if a vitamin or mineral is in short supply, the body prioritizes its use for essential functions. These functions are likely to be oriented to short-term benefit. "Non-essential" functions are those more likely to be of benefit to health in the long run.

Here's a recent paper by Ames in which he tested the triage theory: Adaptive dysfunction of selenoproteins from the perspective of the triage theory: why modest selenium deficiency may increase risk of diseases of aging
The triage theory proposes that modest deficiency of any vitamin or mineral (V/M) could increase age-related diseases. V/M-dependent proteins required for short-term survival and/or reproduction (i.e., “essential”) are predicted to be protected on V/M deficiency over other “nonessential” V/M-dependent proteins needed only for long-term health. The result is accumulation of insidious damage, increasing disease risk. We successfully tested the theory against published evidence on vitamin K. Here, we review about half of the 25 known mammalian selenoproteins; all of those with mouse knockout or human mutant phenotypes that could be used as criteria for a classification of essential or nonessential. Five selenoproteins (Gpx4, Txnrd1, Txnrd2, Dio3, and Sepp1) were classified as essential and 7 (Gpx1, Gpx 2, Gpx 3, Dio1, Dio2, Msrb1, and SelN) nonessential. On modest selenium (Se) deficiency, nonessential selenoprotein activities and concentrations are preferentially lost, with one exception (Dio1 in the thyroid, which we predict is conditionally essential).... The same set of age-related diseases and conditions, including cancer, heart disease, and immune dysfunction, are prospectively associated with modest Se deficiency and also with genetic dysfunction of nonessential selenoproteins, suggesting that Se deficiency could be a causal factor, a possibility strengthened by mechanistic evidence. Modest Se deficiency is common in many parts of the world; optimal intake could prevent future disease.
So, it appears that if not enough selenium, a required mineral, is around, then certain enzyme functions will be compromised, leading to cancer, heart disease, and immune dysfunction, the last of which will predispose to infections and cancer.

So for optimal health, one wants to ensure that all nutrients are present. In the case of selenium, one 200 mg dose of selenium once a week should do the job.

Monday, April 14, 2014

How being like a bodybuilder slows aging

Even if you're not a bodybuilder / weightlifter, and if you have no aspirations to be one, but just want to be healthy, give some consideration to the following. Doing the things bodybuilders do and taking the supplements they take can retard aging and give you the muscles and the mitochondria of a much younger person. (And for the ladies, this goes for you too.)

Exercise and nutritional interventions for improving aging muscle health
Skeletal muscle mass declines with age (i.e., sarcopenia) resulting in muscle weakness and functional limitations. Sarcopenia has been associated with physiological changes in muscle morphology, protein and hormonal kinetics, insulin resistance, inflammation, and oxidative stress. The purpose of this review is to highlight how exercise and nutritional intervention strategies may benefit aging muscle. It is well known that resistance exercise training increases muscle strength and size and evidence also suggests that resistance training can increase mitochondrial content and decrease oxidative stress in older adults. Recent findings suggest that fast-velocity resistance exercise may be an effective intervention for older adults to enhance muscle power and functional capacity. Aerobic exercise training may also benefit aging skeletal muscle by enhancing mitochondrial bioenergetics, improving insulin sensitivity, and/or decreasing oxidative stress. In addition to exercise, creatine monohydrate, milk-based proteins, and essential fatty acids all have biological effects which could enhance some of the physiological adaptations from exercise training in older adults. Additional research is needed to determine whether skeletal muscle adaptations to increased activity in older adults are further enhanced with effective nutritional interventions and whether this is due to enhanced muscle protein synthesis, improved mitochondrial function, and/or a reduced inflammatory response.
So, in addition to resistance training, the authors mention creatine, whey protein ("milk-based proteins"), and omega-3 fats from fish oil ("essential fatty acids"). All of these have anabolic effects and can fight against sarcopenia. Yet these supplements are thought of as for bodybuilders and other athletes only. Nope.

By the way, how serious is sarcopenia? According to this, "A gradual loss of muscle fibres begins at approximately 50 years of age and continues such that by 80 years of age, approximately 50% of the fibres are lost from the limb muscles that have been studied.... 'Master athletes' maintain a high level of fitness throughout their lifespan. Even among master athletes, performance of marathon runners and weight lifters declines after approximately 40 years of age, with peak levels of performance decreased by approximately 50% by 80 years of age."

As for increase in mitochondrial dysfunction and decrease in mitochondrial number, this is though to be a key component of aging. Exercise and appropriate supplements keep mitochondria in well-tuned state and cause an increase or prevent a decrease in their numbers. As far as feeling healthy and energetic, keeping mitochondria well-functioning may be one of the best things you can do.

So, after the age of 40, you need to be doing something about aging in general and loss of muscle mass in particular. Supplements that are though of as being for bodybuilders and other strength athletes - whey and creatine - as well as another one that has anabolic properties - fish oil - are in fact healthy supplements for anyone who's aging (Which is about everybody.) And the exercise that bodybuilders use, weightlifting, is also one of the best things anyone can do for their health.

Sunday, April 13, 2014

High amount of sedentary time may cause six-fold increase in mortality risk

Association of Sedentary Time with Mortality Independent of Moderate to Vigorous Physical Activity
Background

Sedentary behavior has emerged as a novel health risk factor independent of moderate to vigorous physical activity (MVPA). Previous studies have shown self-reported sedentary time to be associated with mortality; however, no studies have investigated the effect of objectively measured sedentary time on mortality independent of MVPA. The objective our study was to examine the association between objectively measured sedentary time and all-cause mortality....

Results

Over an average follow-up of 2.8 years, there were 145 deaths reported. In a model adjusted for sociodemographic factors, lifestyle factors, multiple morbidities, mobility limitation, and MVPA, participants in third quartile (hazard ratio (HR):4.05; 95%CI:1.55–10.60) and fourth quartile (HR:5.94; 95%CI: 2.49–14.15) of having higher percent sedentary time had a significantly increased risk of death compared to those in the lowest quartile.

Conclusions

Our study suggests that sedentary behavior is a risk factor for mortality independent of MVPA. Further investigation, including studies with longer follow-up, is needed to address the health consequences of sedentary behavior.
Note that the model adjusted for other factors, including vigorous exercise, so that one can't count on exercise to save you from the results of sedentary behavior. As they say, sitting is the new smoking. A standing desk makes sense in this regard, as well as standing for other activities.

Saturday, April 12, 2014

Magnesium increases T levels

Effects of Magnesium Supplementation on Testosterone Levels of Athletes and Sedentary Subjects at Rest and after Exhaustion
This study was performed to assess how 4 weeks of magnesium supplementation and exercise affect the free and total plasma testosterone levels of sportsmen practicing tae kwon do and sedentary controls at rest and after exhaustion. The testosterone levels were determined at four different periods: resting before supplementation, exhaustion before supplementation, resting after supplementation, and exhaustion after supplementation in three study groups, which are as follows: Group 1—sedentary controls supplemented with 10 mg magnesium per kilogram body weight. Group 2—tae kwon do athletes practicing 90–120 min/day supplemented with 10 mg magnesium per kilogram body weight. Group 3—tae kwon do athletes practicing 90–120 min/day receiving no magnesium supplements. The free plasma testosterone levels increased at exhaustion before and after supplementation compared to resting levels. Exercise also increased testosterone levels relative to sedentary subjects. Similar increases were observed for total testosterone. Our results show that supplementation with magnesium increases free and total testosterone values in sedentary and in athletes. The increases are higher in those who exercise than in sedentary individuals.
Magnesium is the nutritional factor most people are likely to be deficient in. Some studies have indicated that as many as 60% of Americans are deficient. One reason is that people used to get much of their magnesium through drinking hard water, but hardly anyone does that anymore. Supplementing with magnesium is also crucial for treating chronic fatigue. (As discussed in my book.) Many forms of magnesium are poorly absorbed. Magnesium oxide is the form found most commonly such as in drugstores, and it has nearly zero absorption from the gut. So if you want to supplement, get a form that's readily absorbed; magnesium citrate is best for this.

Friday, April 11, 2014

Chocolate is an exercise mimetic

(–)-Epicatechin enhances fatigue resistance and oxidative capacity in mouse muscle
Abstract  The flavanol (–)-epicatechin, a component of cacao (cocoa), has been shown to have multiple health benefits in humans. Using 1-year-old male mice, we examined the effects of 15 days of (–)-epicatechin treatment and regular exercise on: (1) exercise performance, (2) muscle fatigue, (3) capillarity, and (4) mitochondrial biogenesis in mouse hindlimb and heart muscles. Twenty-five male mice (C57BL/6N) were randomized into four groups: (1) water, (2) water–exercise (W-Ex), (3) (–)-epicatechin ((–)-Epi), and (4) (–)-epicatechin–exercise ((–)-Epi-Ex). Animals received 1 mg kg−1 of (–)-epicatechin or water (vehicle) via oral gavage (twice daily). Exercise groups underwent 15 days of treadmill exercise. Significant increases in treadmill performance (∼50%) and enhanced in situ muscle fatigue resistance (∼30%) were observed with (–)-epicatechin. Components of oxidative phosphorylation complexes, mitofilin, porin, nNOS, p-nNOS, and Tfam as well as mitochondrial volume and cristae abundance were significantly higher with (–)-epicatechin treatment for hindlimb and cardiac muscles than exercise alone. In addition, there were significant increases in skeletal muscle capillarity. The combination of (–)-epicatechin and exercise resulted in further increases in oxidative phosphorylation-complex proteins, mitofilin, porin and capillarity than (–)-epicatechin alone. These findings indicate that (–)-epicatechin alone or in combination with exercise induces an integrated response that includes structural and metabolic changes in skeletal and cardiac muscles resulting in greater endurance capacity. These results, therefore, warrant the further evaluation of the underlying mechanism of action of (–)-epicatechin and its potential clinical application as an exercise mimetic.
It's shown here that chocolate functions as an exercise mimetic, i.e. it provides many of the same benefits, such as improved mitochondrial function and increased capillaries in muscle tissue. Also notable from the study above is that the effects of exercise and epicatechin together were additive, so even if you already exercise, chocolate may provide additional health benefits.

Thursday, April 10, 2014

Association between scales, disordered eating, and weight gain

The association between the development of weighing technology, possession and use of weighing scales, and self-reported severity of disordered eating
D. J. Walsh, B. G. Charlton

The aim of this study is to investigate David Healy’s hypothesis that the development of weighing technologies significantly contributes to the development of anorexia nervosa. A newly developed questionnaire and the EAT-26 were used to investigate these ideas. The key results from this study are that a positive correlation between EAT-26 scores and the frequency of weighing (p ≤ 0.001), and that group differences were also found between the control group and those with an EAT-26 score of 20 or above on weighing scale ownership (p = 0.017), the type of scale owned (p = 0.002) and whether people weighed themselves often (p ≤ 0.001); indicating that those with a higher EAT-26 score were more likely to own weighing scales, own digital weighing scales, and weigh themselves more often. These results suggest that the increased precision and usage of weighing technologies may potentially be a causal factor in disordered eating, and as such, this idea can be extended to suggest the hypothesis that frequent and precise weighing of anorexic patients in therapy may actually be counter-productive.
The idea may perhaps also be extended by suggesting that weight loss in the overweight may be more readily achieved with frequent and precise weighing, though that idea would need to be tested.

Actually, I came across a paper that states that regular weighing may be important for weight loss: Weight-Loss Maintenance for 10 Years in the National Weight Control Registry. This study looked at successful weight-losers from the registry mentioned. It found:
Results
Mean weight loss was 31.3 kg (95% CI=30.8, 31.9) at baseline, 23.8 kg (95% CI=23.2, 24.4) at 5 years and 23.1±0.4 kg (95% CI=22.3, 23.9) at 10 years. More than 87% of participants were estimated to be still maintaining at least a 10% weight loss at Years 5 and 10. Larger initial weight losses and longer duration of maintenance were associated with better long-term outcomes. Decreases in leisure-time physical activity, dietary restraint, and frequency of self-weighing and increases in percentage of energy intake from fat and disinhibition were associated with greater weight regain.

Conclusions
The majority of weight lost by NWCR members is maintained over 10 years. Long-term weight-loss maintenance is possible and requires sustained behavior change.
So, successful weight loss is associated with weighing oneself often, just as might be suspected.

Does soy consumption affect male reproductive parameters?

There's some question as to whether soy consumption affects male reproductive parameters such as sperm count and testosterone levels, some studies answering in the positive, some not. But there are enough studies showing an effect that it's cause for concern. For instance: Inverse Association of Soy Product Intake With Serum Androgen and Estrogen Concentrations in Japanese Men
Serum estradiol concentration was significantly inversely correlated with soy product intake (r = -0.32, p = 0.009), and serum estrone concentration was nonsignificantly inversely correlated with soy product intake (r = -0.24, p = 0.05) after controlling for age, body mass index, smoking status, and ethanol intake.
However, the study found only borderline effects on T levels. Still, borderline effects are enough to make me wary.

Hormonal Effects of Soy in Premenopausal Women and Men. This study found little effect on hormones or sperm counts.

But this one found a large effect on sperm count: Soy food and isoflavone intake in relation to semen quality parameters among men from an infertility clinic
RESULTS There was an inverse association between soy food intake and sperm concentration that remained significant after accounting for age, abstinence time, body mass index, caffeine and alcohol intake and smoking. In the multivariate-adjusted analyses, men in the highest category of soy food intake had 41 million sperm/ml less than men who did not consume soy foods (95% confidence interval = –74, –8; P, trend = 0.02). Results for individual soy isoflavones were similar to the results for soy foods and were strongest for glycitein, but did not reach statistical significance. The inverse relation between soy food intake and sperm concentration was more pronounced in the high end of the distribution (90th and 75th percentile) and among overweight or obese men. Soy food and soy isoflavone intake were unrelated to sperm motility, sperm morphology or ejaculate volume.

CONCLUSIONS These data suggest that higher intake of soy foods and soy isoflavones is associated with lower sperm concentration.
An animal study found large effects on T:
Plasma testosterone and androstenedione levels were significantly lower in the animals fed the phytoestrogen-rich diet compared with animals fed the phytoestrogen-free diet. However, there were no significant differences in plasma LH or estradiol levels between the diet groups. Testicular StAR levels were not significantly different between the phytoestrogen-rich vs the phytoestrogen-free fed animals. These results indicated that consumption of dietary phytoestrogens resulting in very high plasma isoflavone levels over a relatively short period can significantly alter body and prostate weight and plasma androgen hormone levels without affecting gonadotropin or testicular StAR levels.
All in all, I would (and do) avoid soy consumption.

Tuesday, April 8, 2014

Exercise a powerful antidote to aging and fatigue

One of the most prominent characteristics of aging, so prominent that it's thought by many researchers to be the most important factor, is loss of mitochondrial function and biogenesis. However, there's some question whether that is due to aging itself or to the inactivity that goes with aging. The answer appears to be that a lot of it is due to inactivity. Aberrant Mitochondrial Homeostasis in the Skeletal Muscle of Sedentary Older Adults
The role of mitochondrial dysfunction and oxidative stress has been extensively characterized in the aetiology of sarcopenia (aging-associated loss of muscle mass) and muscle wasting as a result of muscle disuse. What remains less clear is whether the decline in skeletal muscle mitochondrial oxidative capacity is purely a function of the aging process or if the sedentary lifestyle of older adult subjects has confounded previous reports. The objective of the present study was to investigate if a recreationally active lifestyle in older adults can conserve skeletal muscle strength and functionality, chronic systemic inflammation, mitochondrial biogenesis and oxidative capacity, and cellular antioxidant capacity. To that end, muscle biopsies were taken from the vastus lateralis of young and age-matched recreationally active older and sedentary older men and women (N = 10/group; ♀ = ♂). We show that a physically active lifestyle is associated with the partial compensatory preservation of mitochondrial biogenesis, and cellular oxidative and antioxidant capacity in skeletal muscle of older adults. Conversely a sedentary lifestyle, associated with osteoarthritis-mediated physical inactivity, is associated with reduced mitochondrial function, dysregulation of cellular redox status and chronic systemic inflammation that renders the skeletal muscle intracellular environment prone to reactive oxygen species-mediated toxicity. We propose that an active lifestyle is an important determinant of quality of life and molecular progression of aging in skeletal muscle of the elderly, and is a viable therapy for attenuating and/or reversing skeletal muscle strength declines and mitochondrial abnormalities associated with aging.
Exercise is a powerful antidote to aging.

In my book (see sidebar), I show that aging and chronic fatigue have many factors in common, that is, they are "comorbid". Mitochondrial dysfunction is one of those comorbidities, and exercise (among other things) improves mitochondrial function and ameliorates both aging and chronic fatigue.

Monday, April 7, 2014

Weightlifting for the frail elderly doubled muscle strength

Exercise Training and Nutritional Supplementation for Physical Frailty in Very Elderly People
METHODS
We conducted a randomized, placebo-controlled trial comparing progressive resistance exercise training, multinutrient supplementation, both interventions, and neither in 100 frail nursing home residents over a 10-week period.
RESULTS
The mean (±SE) age of the 63 women and 37 men enrolled in the study was 87.1 ±0.6 years (range, 72 to 98); 94 percent of the subjects completed the study. Muscle strength increased by 113 ±8 percent in the subjects who underwent exercise training, as compared with 3 ±9 percent in the nonexercising subjects (P<0.001). Gait velocity increased by 11.8 ±3.8 percent in the exercisers but declined by 1.0 ±3.8 percent in the nonexercisers (P = 0.02). Stair-climbing power also improved in the exercisers as compared with the nonexercisers (by 28.4 ±6.6 percent vs. 3.6 ±6.7 percent, P = 0.01), as did the level of spontaneous physical activity. Cross-sectional thigh-muscle area increased by 2.7 ±1.8 percent in the exercisers but declined by 1.8 ±2.0 percent in the nonexercisers (P = 0.11). The nutritional supplement had no effect on any primary outcome measure. Total energy intake was significantly increased only in the exercising subjects who also received nutritional supplementation. CONCLUSIONS High-intensity resistance exercise training is a feasible and effective means of counteracting muscle weakness and physical frailty in very elderly people. In contrast, multinutrient supplementation without concomitant exercise does not reduce muscle weakness or physical frailty.
This article has been cited over 2100 times.

The nutritional intervention produced no change in the results, but according to the full paper, it consisted of a 360 calorie liquid that was 60% carbohydrate, 23% fat, and 17% soy protein, and was mainly designed to augment calories and vitamins and minerals. That's only about 14 grams of protein extra daily. So I wouldn't expect that to do much. They might have seen better results with a whey shake a couple times a day.

That being said, the results were remarkable and show, I think, that much of the pathology of aging is due to inactivity, disuse, and atrophy. If every adult lifted weights, they could avoid or greatly delay entrance into a nursing home, especially since muscle weakness is a prime cause of frailty and being unable to care for oneself.

Sunday, April 6, 2014

More muscle, better health

The underappreciated role of muscle in health and disease
Muscle plays a central role in whole-body protein metabolism by serving as the principal reservoir for amino acids to maintain protein synthesis in vital tissues and organs in the absence of amino acid absorption from the gut and by providing hepatic gluconeogenic precursors. Furthermore, altered muscle metabolism plays a key role in the genesis, and therefore the prevention, of many common pathologic conditions and chronic diseases. Nonetheless, the maintenance of adequate muscle mass, strength, and metabolic function has rarely, if ever, been targeted as a relevant endpoint of recommendations for dietary intake. It is therefore imperative that factors directly related to muscle mass, strength, and metabolic function be included in future studies designed to demonstrate optimal lifestyle behaviors throughout the life span, including physical activity and diet.
Muscle "breathes" amino acids - it builds itself up after feeding, and breaks down during fasting to maintain homeostatic levels of amino acids in the blood. Without doing that, you would soon be dead. It follows (so I think) that having more muscle is better for overall health than having less muscle, but this fact is definitely "underappreciated". Sarcopenia is the condition in later life or illness when there is not enough muscle. Besides being conducive to disability and falls (with subsequent bone breakage), sarcopenia also means that amino acid homeostasis is harder to maintain. Oxidative stress, seen at much higher levels in older people, is the result.

So should everyone lift weights? I think so. It's been shown to be of benefit to people as old as in their 90s - of course older people will need special help and supervision - and it's also being advocated for children.

One interesting item from the above paper is that it's possible that the RDA for protein is too low.
The optimal intake of protein is uncertain, but one can derive estimates from acute metabolic studies of muscle metabolism. Thus, the maximal response of muscle protein synthesis can be attained with intake of ≈15 g essential amino acids (EAAs) (91), which is approximately equal to the amount of EAAs in the EAR for a 55-kg woman (0.66 g protein · kg−1 · d−1 × 55 kg × 0.42 EAA/g protein = 15.2 g protein). The response to a single dose of amino acids can potentially be achieved multiple times per day, with additive effects, with repeated meal ingestion (91, 92). Consequently, it would not be unreasonable to expect beneficial effects stemming from increased myofibrillar and mitochondrial protein synthesis to be achieved with the ingestion of 15 g EAAs at each meal rather than at only one meal per day. This would translate to a protein intake as high as 1.8 g protein · kg−1 · d−1. Although this amount may seem extreme in the context of the current recommendations, it is in line with the amount of protein in the average American diet, which was reported in the DRIs to be 1.5 g · kg−1 · d−1 for adults (62). Furthermore, detrimental effects of protein intakes ≥2.0 g · kg−1 · d−1 have not been documented (62).
If this line of reasoning is correct, virtually everyone should be eating protein in amounts closer to that of bodybuilders.

Saturday, April 5, 2014

Maximum BMI shows increased risk of obesity

Using maximum weight to redefine body mass index categories in studies of the mortality risks of obesity
Background

The high prevalence of disease and associated weight loss at older ages limits the validity of prospective cohort studies examining the association between body mass index (BMI) and mortality.
Methods

I examined mortality associated with excess weight using maximum BMI—a measure that is robust to confounding by illness-induced weight loss. Analyses were carried out on US never-smoking adults ages 50-84 using data from the National Health and Nutrition Examination Surveys (1988-1994 and 1999-2004) linked to the National Death Index through 2006. Cox models were used to estimate hazard ratios for mortality according to BMI at time of survey and at maximum.
Results

Using maximum BMI, hazard ratios for overweight (BMI, 25.0-29.9 kg/m2), obese class 1 (BMI, 30.0-34.9 kg/m2) and obese class 2 (BMI, 35.0 kg/m2 and above) relative to normal weight (BMI, 18.5-24.9 kg/m2) were 1.28 (95% confidence interval [CI], 0.89-1.84), 1.67 (95% CI, 1.15-2.40), and 2.15 (95% CI, 1.47-3.14), respectively. The corresponding hazard ratios using BMI at time of survey were 0.98 (95% CI, 0.77-1.24), 1.18 (95% CI, 0.91-1.54), and 1.31 (95% CI, 0.95-1.81). The percentage of mortality attributable to overweight and obesity among never-smoking adults ages 50-84 was 33% when assessed using maximum BMI. The comparable figure obtained using BMI at time of survey was substantially smaller at 5%. The discrepancy in estimates is explained by the fact that when using BMI at time of survey, the normal category combines low-risk stable-weight individuals with high-risk individuals that have experienced weight loss. In contrast, only the low-risk stable-weight group is categorized as normal weight using maximum BMI.
Conclusions

Use of maximum BMI reveals that estimates based on BMI at the time of survey may substantially underestimate the mortality burden associated with excess weight in the US.
If this is correct, and I see no reason why it's not, then the mortality risk of obesity has been greatly underestimated. The key point is that some illnesses cause weight loss, thus skewing the statistics, i.e. more normal weight people ill, fewer overweight. Eliminate that problem, and the true risk of obesity rises.

Friday, April 4, 2014

Creatine prevents fat accumulation in liver

Creatine Supplementation Prevents the Accumulation of Fat in the Livers of Rats Fed a High-Fat Diet
The aim of the present study was to examine the effects of creatine supplementation on liver fat accumulation induced by a high-fat diet in rats. Rats were fed 1 of 3 different diets for 3 wk: a control liquid diet (C), a high-fat liquid diet (HF), or a high-fat liquid diet supplemented with creatine (HFC). The C and HF diets contained, respectively, 35 and 71% of energy derived from fat. Creatine supplementation involved the addition of 1% (wt:v) of creatine monohydrate to the liquid diet. The HF diet increased total liver fat concentration, liver TG, and liver TBARS and decreased the hepatic S-adenosylmethionine (SAM) concentration. Creatine supplementation normalized all of these perturbations. Creatine supplementation significantly decreased the renal activity of l-arginine:glycine amidinotransferase and plasma guanidinoacetate and prevented the decrease in hepatic SAM concentration in rats fed the HF diet. However, there was no change in either the phosphatidylcholine:phosphatidylethanolamine (PE) ratio or PE N-methyltransferase activity. The HF diet decreased mRNA for PPAR╬▒ as well as 2 of its targets, carnitine palmitoyltransferase and long-chain acylCoA dehydrogenase. Creatine supplementation normalized these mRNA levels. In conclusion, creatine supplementation prevented the fatty liver induced by feeding rats a HF diet, probably by normalization of the expression of key genes of ╬▓-oxidation.
I don't know whether creatine supplementation would have this effect in a human who is metabolically normal, but since creatine does increase strength and maximal power, it perhaps does so by increasing expression of genes responsible for fat metabolism.

Serum BDNF negatively correlated with treatment failure in depression

Brain-derived neurotrophic factor (BDNF) is a protein that helps regulate brain and nervous tissue growth and plasticity, and low levels of it have been implicated in depression. For instance, the rapid effect of wake therapy (sleep deprivation) in depression seems to be correlated with BDNF levels. One study found that a failure of BDNF to rise with antidepressant drug treatment predicted treatment failure. The early non-increase of serum BDNF predicts failure of antidepressant treatment in patients with major depression: A pilot study
In the treatment of patients with major depressive disorder (MDD), early non-improvement of symptoms after initiation of antidepressant treatment is a highly sensitive and specific marker for final treatment failure. On the other hand, meta-analyses of clinical studies investigating serum BDNF (sBDNF) concentration before and after antidepressant treatment showed an increase of sBDNF during treatment, which was correlated with amelioration of depressive symptoms. No study has yet investigated the predictive value of early changes of sBDNF for final treatment outcome of the individual patient. The aim of this study was to investigate in patients with MDD, whether i) the non-increase of sBDNF in the early course of treatment is a specific and sensitive marker for final treatment failure, ii) whether the sensitivity and specificity of early non-improvement for treatment failure can be increased by combining it with the marker “early non-increase of sBDNF”. For this purpose, we performed a pilot study with 41 inpatients with MDD according to DSM-IV, who were treated in a naturalistic setting. Depression severity and sBDNF were measured in weekly intervals from baseline to week six with the 21-item Hamilton Depression Rating Scale (HAMD-21) and ELISA, respectively. The individual markers sBDNF non-increase and HAMD-21 non-improvement from baseline to day 7 or 14 predicted later non-response and non-remission with moderate to high specificity. The combined marker sBDNF non-increase plus HAMD-21 non-improvement at day 14 increased the specificity for non-response and non-remission to 100%. Our data provide the first evidence that the absence of an early increase of sBDNF in conjunction with early non-improvement might be a highly specific peripheral marker predictive for treatment failure in patients with MDD. If replicated, this combined marker could be considered useful for prospective confirmatory trials in patients with MDD.
Seems as if BDNF is closely and negatively correlated with depression.

To speculate a bit, exercise is known to be effective in treating depression, and exercise increases BDNF levels as well as increasing growth of neurons. This would also seem to put the kibosh on neurotransmitter theories of depression.

Thursday, April 3, 2014

Testosterone, fatigue, energy

One of the symptoms of low testosterone (T), also known as hypogonadism, is fatigue or low energy levels. A couple of papers give some insight into how this works, as well as the extent to which replacing T contributes to higher energy.

Voluntary running, skeletal muscle gene expression, and signaling inversely regulated by orchidectomy and testosterone replacement
Declines in skeletal muscle size and strength, often seen with chronic wasting diseases, prolonged or high-dose glucocorticoid therapy, and the natural aging process in mammals, are usually associated with reduced physical activity and testosterone levels. However, it is not clear whether the decline in testosterone and activity are causally related. Using a mouse model, we found that removal of endogenous testosterone by orchidectomy results in an almost complete cessation in voluntary wheel running but only a small decline in muscle mass. Testosterone replacement restored running behavior and muscle mass to normal levels. Orchidectomy also suppressed the IGF-I/Akt pathway, activated the atrophy-inducing E3 ligases MuRF1 and MAFBx, and suppressed several energy metabolism pathways, and all of these effects were reversed by testosterone replacement. The study also delineated a distinct, previously unidentified set of genes that is inversely regulated by orchidectomy and testosterone treatment. These data demonstrate the necessity of testosterone for both speed and endurance of voluntary wheel running in mice and suggest a potential mechanism for declined activity in humans where androgens are deficient.
In this study, castrated mice who had their T replaced engaged in voluntary running at more than three times the amount that untreated mice did.

Relationship Between Testosterone Levels, Insulin Sensitivity, and Mitochondrial Function in Men. In this study, low T was associated with insulin resistance and low aerobic capacity, which appears to be related to mitochondrial function.

So overall, it seems that one of the pathways through which T works is improved mitochondrial function. If you've read my book (see sidebar), you know that mitochondrial dysfunction is one of the main ways through which fatigue is produced in illness. Higher T levels can help this, perhaps even when other causes of fatigue are at work.

The lesson here is that, if you're a man and have low energy levels or even outright chronic fatigue, you must ensure that T levels are normal. A doctor can check this.

Lifestyle influences on sperm production

Lifestyle impact and the biology of the human scrotum
The possession of a scrotum to contain the male gonads is a characteristic feature of almost all mammals, and appears to have evolved to allow the testes and epididymis to be exposed to a temperature a few degrees below that of core body temperature. Analysis of cryptorchid patients, and those with varicocele suggest that mild scrotal warming can be detrimental to sperm production, partly by effects on the stem cell population, and partly by effects on later stages of spermatogenesis and sperm maturation. Recent studies on the effects of clothing and lifestyle emphasize that these can also lead to chronically elevated scrotal temperatures. In particular, the wearing of nappies by infants is a cause for concern in this regard. Together all of the evidence indirectly supports the view that lifestyle factors in addition to other genetic and environmental influences could be contributing to the secular trend in declining male reproductive parameters. The challenge will be to provide relevant and targeted experimental results to support or refute the currently circumstantial evidence.
From the full article we learn:
Normal scrotal temperature (the external surface of the scrotum) is approximately 34°C in a normally clothed man walking about or maintaining a loose stance, and it has been estimated that testicular temperature within the scrotum is between 0.1 and 0.6°C higher than this [32,35,36]. Clothing itself appears to contribute about 0.5–1.0°C [37], compared to being naked. Clothed and sitting down with thighs apart raises scrotal temperature to about 35 C, whereas sitting with thighs together quickly allows scrotal temperature to rise to above 36 C, i.e. to abdominal temperature within the testis [36]. Several studies have now shown that men with predominantly sedentary occupations [36], or who spend considerable time driving a vehicle [38,39], have higher average scrotal temperatures and consequently lower average sperm production or reduced fertility.
This gives scientific cred to the manosphere observation that a man should not sit with his legs crossed, since it makes him appear less manly and less confident. According to this article, sitting legs crossed may literally make one less of a man, if by that we include measures of sperm production.

Don't wear skinny jeans, as if you didn't have reason enough already not to wear them.

This also gives new impetus to the use of standing desks.