More On Sugar And Obesity

Here is yet another study linking sugar and sweetened beverages to obesity.  The importance of avoiding excess sugar consumption and of avoiding drinking empty calories is underscored here. These sorts of dietary changes can have a large impact on overall health.

Health Effects Of A Low Sodium Diet

What are the health effects of a low sodium diet? Abstract conclusions:

AUTHORS' CONCLUSIONS:

Sodium reduction from an average high usual sodium intake level (201 mmol/day) to an average level of 66 mmol/day, which is below the recommended upper level of 100 mmol/day (5.8 g salt), resulted in a decrease in SBP/DBP of 1/0 mmHg in white participants with normotension and a decrease in SBP/DBP of 5.5/2.9 mmHg in white participants with hypertension. A few studies showed that these effects in black and Asian populations were greater. The effects on hormones and lipids were similar in people with normotension and hypertension. Renin increased 1.60 ng/mL/hour (55%); aldosterone increased 97.81 pg/mL (127%); adrenalin increased 7.55 pg/mL (14%); noradrenalin increased 63.56 pg/mL: (27%); cholesterol increased 5.59 mg/dL (2.9%); triglyceride increased 7.04 mg/dL (6.3%).

Low sodium helps decrease blood pressure but for some reason cholesterol and triglycerides were increased. More study is required.

Sweetness, Food Addiction, And Overweight: A Study Denying A Connection?

Here is a paper from several years ago that goes against "conventional wisdom" arguing that:

...sugary foods contribute minimally to 'food dependence' and increased risk of weight gain. Instead, they are consistent with the current scientific notion that food energy density, and the unique individual experience of eating, plays an important role in determining the reward value of food and promoting excessive energy intake.

I think we need to look at additional studies for conformation or refutation, considering the importance of sugar in the American diet and American obesity.  No doubt of course "high food density" is the most important thing and a combination of high fat and sweetness - indeed identified in this study as a problem - may be a particular "villain" here.

Protein Intake Timing

Here is a paper from several years ago that asserts that protein intake distribution – consuming most of the protein at one meal or spreading it out more evenly throughout the day – does not affect muscle building.  Hence the authors conclude:

We conclude that over an 8-week intervention period, the protein intake distribution pattern in mixed meals does not play an important role in determining anabolic response, muscle strength, or functional outcomes. 

One caveat is that it is uncertain whether the subjects were doing any resistance exercising. For example, you may expect to observe better results consuming a lot of protein just after the workout (and/or before and after) than distributed throughout the day, but this needs to be confirmed.  If the subjects were just regularly active, then perhaps intake time does not matter.  More study is required.

Meal Delivery And Elder Feeding

Home-delivered meal programs help elder diets, abstract:

BACKGROUND:

Poor diet quality and insufficient nutrient intake is of particular concern among older adults. The Older Americans Act of 1965 authorizes home-delivered meal services to homebound individuals aged 60 years and older.

OBJECTIVE:

The purpose of this study was to review scientific evidence on the impact of home-delivered meal services on diet and nutrition among recipients.

METHODS:

Keyword and reference searches were conducted in Cochrane Library, Google Scholar, PubMed and Web of Science. Inclusion criteria included: study design (randomized controlled trials, cohort studies, pre-post studies, or cross-sectional studies); main outcome (food and nutrient intakes); population (home-delivered meal program participants); country (US); language (articles written in English); and article type (peer-reviewed publications or theses).

RESULTS:

Eight studies met the inclusion criteria, including two randomized controlled trial studies (from the same intervention), one cohort study, two pre-post studies, and three cross-sectional studies. All but two studies found home-delivered meal programs to significantly improve diet quality, increase nutrient intakes, and reduce food insecurity and nutritional risk among participants. Other beneficial outcomes include increased socialization opportunities, improvement in dietary adherence, and higher quality of life.

CONCLUSIONS:

Home-delivered meal programs improve diet quality and increase nutrient intakes among participants. These programs are also aligned with the federal cost-containment policy to rebalance long-term care away from nursing homes to home- and community-based services by helping older adults maintain independence and remain in their homes and communities as their health and functioning decline.

As families are scattered about, particularly in the USA, it is important that some infrastructure exists to ensure older people have adequate dietary intake.

Resistance Training Restores Muscle Sensitivity To Feeding

An interesting paper on exercise, feeding, and muscle; abstract:

Normally, skeletal muscle mass is unchanged, beyond periods of growth, but it begins to decline in the fourth or fifth decade of life. The mass of skeletal muscle is maintained by ingestion of protein-containing meals. With feeding, muscle protein synthesis (MPS) is stimulated and a small suppression of muscle protein breakdown (MPB) occurs, such that protein balance becomes positive (MPS>MPB). As the postprandial period subsides and a transition toward fasting occurs, the balance of muscle protein turnover becomes negative again (MPB>MPS). Thus, during maintenance of skeletal muscle mass, the long-term net result is that MPS is balanced by MPB. Acutely, however, it is of interest to determine what regulates feeding-induced increases in MPS, since it appears that, in a number of scenarios (for example aging, disuse, and wasting diseases), a suppression of MPS in response to feeding is a common finding. In fact, recent findings point to the fact that loss of skeletal muscle mass with disuse and aging is due not chronic changes in MPS or MPB, but to a blunted feeding-induced rise in MPS. Resistance exercise is a potent stimulator of MPS and appears to synergistically enhance the gains stimulated by feeding. As such, resistance exercise is an important countermeasure to disuse atrophy and to age-related declines in skeletal muscle mass. What is less well understood is how the intensity and volume of the resistance exercise stimulus is sufficient to result in rises in MPS. Recent advances in this area are discussed here, with a focus on human in vivo data.

To summarize: feeding, particularly of protein, favors muscle buildup as opposed t breakdown and fasting does the opposite.  Muscle loss with age seems linked to suppressed muscle buildup from feeding and this suppression can be reduced by resistance training.  Therefore, resistance training helps to reduce/prevent age-related muscle loss, possibly through enhancing feeding-related stimulation of muscle protein synthesis.  Hence the importance of resistance training and (protein) feeding (albeit of course not in excess).

Coffee And Cancer Risk

Here is a paper on coffee consumption and cancer risk from several years ago,  Bottom like is that there doesn't seem to be a big effect either way; coffee can cause decreased risk for some cancers, but possibly increased risk for childhood leukemia with maternal coffee drinking during pregnancy. The data are "limited and inconsistent" in some cases; overall it seems like a "wash" based on these findings, no big effect. Abstract:

We reviewed available evidence on coffee drinking and the risk of all cancers and selected cancers updated to May 2016. Coffee consumption is not associated with overall cancer risk. A meta-analysis reported a pooled relative risk (RR) for an increment of 1 cup of coffee/day of 1.00 [95% confidence interval (CI): 0.99-1.01] for all cancers. Coffee drinking is associated with a reduced risk of liver cancer. A meta-analysis of cohort studies found an RR for an increment of consumption of 1 cup/day of 0.85 (95% CI: 0.81-0.90) for liver cancer and a favorable effect on liver enzymes and cirrhosis. Another meta-analysis showed an inverse relation for endometrial cancer risk, with an RR of 0.92 (95% CI: 0.88-0.96) for an increment of 1 cup/day. A possible decreased risk was found in some studies for oral/pharyngeal cancer and for advanced prostate cancer. Although data are mixed, overall, there seems to be some favorable effect of coffee drinking on colorectal cancer in case-control studies, in the absence of a consistent relation in cohort studies. For bladder cancer, the results are not consistent; however, any possible direct association is not dose and duration related, and might depend on a residual confounding effect of smoking. A few studies suggest an increased risk of childhood leukemia after maternal coffee drinking during pregnancy, but data are limited and inconsistent. Although the results of studies are mixed, the overall evidence suggests no association of coffee intake with cancers of the stomach, pancreas, lung, breast, ovary, and prostate overall. Data are limited, with RR close to unity for other neoplasms, including those of the esophagus, small intestine, gallbladder and biliary tract, skin, kidney, brain, thyroid, as well as for soft tissue sarcoma and lymphohematopoietic cancer.

I don't drink coffee myself, but based on these data overall it seems not do any harm taking all risks together - although pregnant women may want to ask their doctor about the risk in that specific case.

Dietary Lapses

What is the frequency and predictors of dietary lapses?  A paper from several years ago looks into this, abstract:

BACKGROUND:

Adherence to dietary prescriptions is critical for successful weight loss and weight loss maintenance. However, research on specific instances of inadherence (lapses) is limited, and findings regarding the frequency, nature, and causes of lapses are mixed. Additionally, no studies have examined lapses over the course of a weight loss program.

PURPOSE:

In the context of a reduced calorie diet prescribed as part of a behavioral treatment, we aimed to characterize lapse occurrence, examine lapse frequency across treatment, examine predictors of lapses, and assess the relationship between lapses and weight loss.

METHODS:

Adults (n = 189) enrolled in a 12-month behavioral weight loss program completed ecological momentary assessment (EMA) at baseline, mid-treatment, and end of treatment. At each EMA survey, participants indicated whether a lapse had occurred, and responded to questions assessing situational, environmental, and affective states.

RESULTS:

Lapse frequency showed a curvilinear relationship over time, such that frequency first decreased and then increased. Lapse frequency at baseline was negatively associated with early and overall weight loss. Lapses most often occurred at home, in the evenings, on the weekends, and entailed eating a forbidden food. Greater overall levels of assessed affective and environmental triggers predicted lapses, and greater momentary hunger and deprivation, and the presence of palatable food, also prospectively predicted lapses.

CONCLUSIONS:

In addition to characterizing lapse frequency, the current study identified prospective predictors of lapses across treatment. These findings support the importance of lapses to weight control and provide insight for potential targets of intervention to prevent lapse occurrence.

One point I would raise in response to: "Lapses most often occurred at home, in the evenings, on the weekends, and entailed eating a forbidden food. Greater overall levels of assessed affective and environmental triggers predicted lapses, and greater momentary hunger and deprivation, and the presence of palatable food, also prospectively predicted lapses" is to suggest that a pre-planned cheat meal (for those more overweight) or cheat day (or those who cab be more flexible, who have less weight to lose) may alleviate some of these problems.  The key is discipline, not to "cheat" all week.  "Cheating" may help reset metabolism and leptin levels and avoid the slowing of metabolism that accompanies dieting (although this requires more evidence).  The psychological benefits are obvious.

Diet And Cardiometabolic Deaths

From several years ago is a study the emphasizes what we should all hopefully already know - some foods increase the risk of death from cardiovascular events and other foods decrease that risk.  Here is the Results section from the Abstract; I am bold-fonting the important points for ease of reading:

RESULTS:In 2012, 702 308 cardiometabolic deaths occurred in US adults, including 506 100 from heart disease (371 266 coronary heart disease, 35 019 hypertensive heart disease, and 99 815 other cardiovascular disease), 128 294 from stroke (16 125 ischemic, 32 591 hemorrhagic, and 79 578 other), and 67 914 from type 2 diabetes. Of these, an estimated 318 656 (95% uncertainty interval [UI], 306 064-329 755; 45.4%) cardiometabolic deaths per year were associated with suboptimal intakes-48.6% (95% UI, 46.2%-50.9%) of cardiometabolic deaths in men and 41.8% (95% UI, 39.3%-44.2%) in women; 64.2% (95% UI, 60.6%-67.9%) at younger ages (25-34 years) and 35.7% (95% UI, 33.1%-38.1%) at older ages (≥75 years); 53.1% (95% UI, 51.6%-54.8%) among blacks, 50.0% (95% UI, 48.2%-51.8%) among Hispanics, and 42.8% (95% UI, 40.9%-44.5%) among whites; and 46.8% (95% UI, 44.9%-48.7%) among lower-, 45.7% (95% UI, 44.2%-47.4%) among medium-, and 39.1% (95% UI, 37.2%-41.2%) among higher-educated individuals. The largest numbers of estimated diet-related cardiometabolic deaths were related to high sodium (66 508 deaths in 2012; 9.5% of all cardiometabolic deaths), low nuts/seeds (59 374; 8.5%), high processed meats (57 766; 8.2%), low seafood omega-3 fats (54 626; 7.8%), low vegetables (53 410; 7.6%), low fruits (52 547; 7.5%), and high SSBs (51 694; 7.4%). Between 2002 and 2012, population-adjusted US cardiometabolic deaths per year decreased by 26.5%. The greatest decline was associated with insufficient polyunsaturated fats (-20.8% relative change [95% UI, -18.5% to -22.8%]), nuts/seeds (-18.0% [95% UI, -14.6% to -21.0%]), and excess SSBs (-14.5% [95% UI, -12.0% to -16.9%]). The greatest increase was associated with unprocessed red meats (+14.4% [95% UI, 9.1%-19.5%]).

Talk to your physician about adjusting your diet accordingly. SSBs = sugar-sweetened beverages.

A Gentleman's Agreement

Another article about the gut microbiota and immunity is here.  Abstract:

Our body is colonized by more than a hundred trillion commensals, represented by viruses, bacteria and fungi. This complex interaction has shown that the microbiome system contributes to the host's adaptation to its environment, providing genes and functionality that give flexibility of diet and modulate the immune system in order not to reject these symbionts. In the intestine, specifically, the microbiota helps developing organ structures, participates of the metabolism of nutrients and induces immunity. Certain components of the microbiota have been shown to trigger inflammatory responses, whereas others, anti-inflammatory responses. The diversity and the composition of the microbiota, thus, play a key role in the maintenance of intestinal homeostasis and explain partially the link between intestinal microbiota changes and gut-related disorders in humans. Tight junction proteins are key molecules for determination of the paracellular permeability. In the context of intestinal inflammatory diseases, the intestinal barrier is compromised, and decreased expression and differential distribution of tight junction proteins is observed. It is still unclear what is the nature of the luminal or mucosal factors that affect the tight junction proteins function, but the modulation of the immune cells found in the intestinal lamina propria is hypothesized as having a role in this modulation. In this review, we provide an overview of the current understanding of the interaction of the gut microbiota with the immune system in the development and maintenance of the intestinal barrier.

Immunity and maintenance of the intestinal barrier - crucial to health - are strongly affected by the composition of the gut microbiota, which in turn is strongly affected by diet.  High fiber, active culture yogurt - these are part of a healthy diet and can help maintain a better gut profile.

Maintaining Lean Body Mass While "Cutting"

A regimen for maintaining lean body mass while "cutting" for a drug-free physique competition was studied in a female competitor.  Abstract:

To achieve the criterion appearance prior to competing in a physique competition, athletes undergo preparatory regimens involving high-volume intense resistance and aerobic exercise with hypocaloric energy intake. As the popularity of "drug-free" competition increases, more athletes are facing this challenge without the recuperative advantage provided by performance-enhancing drugs. Consequently, the likelihood of loss of lean body and/or bone mass is increased. The purpose of this investigation was to monitor changes in body composition for a 29-year-old self-proclaimed drug-free female figure competitor during a 32-week preparatory regimen comprising high-volume resistance and aerobic exercise with hypocaloric energy intake. We used dual-energy x-ray absorptiometry (DXA) to evaluate regional fat and bone mineral density. During the initial 22 weeks, the subject reduced energy intake and engaged in resistance (4-5 sessions/week) and aerobic (3 sessions/week) training. During the final 10 weeks, the subject increased exercise frequency to 6 (resistance) and 4 (aerobic) sessions/week while ingesting 1130-1380 kcal/day. During this 10-week period, she consumed a high quantity of protein (~55% of energy intake) and nutritional supplements. During the 32 weeks, body mass and fat mass decreased by 12% and 55%, respectively. Conversely, lean body mass increased by 1.5%, an amount that exceeded the coefficient of variation associated with DXA-derived measurement. Total bone mineral density was unchanged throughout. In summary, in preparation for a figure competition, a self-proclaimed drug-free female achieved the low body-fat percentage required for success in competition without losing lean mass or bone density by following a 32-week preparatory exercise and nutritional regimen.

Thus, consistent with popular conception, a high protein intake was associated with maintenance (actually increase) with decreased body mass and fat mass.  High volume exercise and calorie-cutting were all part of the mix, also consistent with popular practice.

Melanesians, Non-Western Diet, And Cardiovascular Disease Risk

Why do some non-Western populations have low rates of stroke and heart disease?  Here is a paper looking at one such population.  Abstract (containing one spelling correction):

OBJECTIVES:

To compare cardiovascular risk factor levels between non-westernized Melanesians, apparently free from stroke and ischaemic heart disease, and healthy Swedish populations, and to analyse, among adult Melanesians, relations with age, sex and smoking status.

DESIGN:

Cross-sectional survey.

SUBJECTS:

(i) Traditional horticulturalists in Kitava, Trobriand Islands, Papua New Guinea, uninfluenced by western diet. this study tested 151 males and 69 females aged 14-87 years with 76% and 80% smokers over 20 years. (ii) Healthy Swedish reference populations.

MAIN OUTCOME MEASURES:

Sitting systolic and diastolic blood pressure, weight, height, body mass index, circumferences of waist, pelvis and mid upper arm, triceps skinfold thickness, fasting serum total cholesterol, triglycerides, high-density lipoprotein cholesterol, estimated low-density lipoprotein cholesterol, apolipoprotein B, apolipoprotein A1 and apolipoprotein (a).

RESULTS:

Compared to Sweden, diastolic blood pressure, body mass index and triceps skinfold thickness were substantially lower in Kitava, where all subjects > or = 40 years were below Swedish medians. Among males > or = 20 and females > or = 60 years systolic blood pressure was lower in Kitavans. Fasting serum total cholesterol, low-density lipoprotein cholesterol and apolipoprotein B were 10-30% lower in Kitavan males > or = 40 and females > or = 60 years. Triglycerides were higher in Kitavans aged 20-39. High-density lipoprotein cholesterol did not differ while apolipoprotein A1 was lower in Kitavans. Apolipoprotein (a) tended to be lower in Kitavans, but the differences were small.

CONCLUSIONS:

Of the analysed variables, leanness and low diastolic blood pressure seem to offer the best explanations for the apparent absence of stroke and ischaemic heart disease in Kitava. The lower serum cholesterol may provide some additional benefit. Differences in dietary habits may explain the findings.

So, dietary differences leading to lean body structure, lower blood pressure, and lower cholesterol levels may explain the better stroke/heart disease profile in Melanesians vs. Swedes.  Of course, genetic differences, not mentioned in this abstract, between the two populations may influence this as well.  What I would like to see is a study comparing people within each population, each group having a different diet.  For example, do Melanesians with a Western diet have higher rates to stroke and heart disease?  What about Swedes on a healthier diet?

What We Eat Is What We Think?

Consider that diet can affect your gut microbiome.  Consider also that gut bacteria produce short chain fatty acids from dietary fiber, so that diet can not only affect what bacterial species are in the gut but what products they produce.  Now, take a look at this article on the “gut-brain axis” mediated in part by lipids, including fatty acids, and this other article on a similar topic.

“We are what we eat,” indeed.  Perhaps, we “think what we eat” as well.

Artificial Sweeteners And Type 2 Diabetes Study

Here is an article on artificial sweeteners and type 2 diabetes risk.  Abstract:

BACKGROUND:

The influence of artificial sweeteners on metabolic diseases is controversial. Artificially sweetened beverages have been associated with an increased risk of type 2 diabetes (T2D) but biases and reverse causation have been suspected to have influenced the observed association. In addition, it has been suggested that investigation into the relationship between the frequency and duration of the consumption of packet or tablet artificial sweeteners and T2D risk is necessary.

METHODS:

We used data from 61,440 women in the prospective E3N-European Prospective Investigation into Cancer and Nutrition study, conducted between 1993 and 2011. We estimated hazards ratios (HRs) and 95% CIs of T2D risk associated with both the frequency and the duration of use of artificial sweeteners consumed in packets or tablets.

RESULTS:

Compared to "never or rare" consumers of artificial sweeteners, those using them "always or almost always" had an increased risk of T2D (HR = 1.83 [95% CI 1.66-2.02] in the multivariate model [MM], HR = 1.33 [95% CI 1.20-1.47] when further adjusted for body mass index, BMI). Women consuming artificial sweeteners in packets or tablets for more than 10 years also had an increased risk of T2D compared to never or rare users (HR = 2.10 [95% CI 1.83-2.40] in the MM and HR = 1.15 [95% CI 1.00-1.33] when adjusted for BMI, respectively).

CONCLUSIONS:

Our data suggest that both a higher frequency and a longer consumption of artificial sweeteners in packets or tablets was associated with T2D risk, independently of major T2D risk factors, but partially mediated by adiposity. A precautionary principle should be applied to the promotion of these products that are still largely recommended as healthy sugar substitutes.

A reasonable strategy may be to not use such artificial sweeteners and cut down on sugar in your diet as well. Avoid diabetes, and your health will thank you for it.

An Optimal Diet?

An article on whether there is an optimal diet for weight management and metabolic health can be found here.

The bottom line is that while different types of diets may stress optimizing different health outcomes (low fat diets helping with LDL; low carb diets helping more with triglycerides and HDL), the main point is to adhere to a healthy diet.  Both low fat and low carb can work; people have different preferences, but if you are overweight, sticking to a diet that results in weight loss will improve many metrics of health and fitness.

Elimination Diets For Neurodevelopmental Disorders.

Elimination diets attempt to identity foods that cause certain symptoms or disorders.  Here is a paper that focuses on elimination diets as interventions for, e.g., attention deficit hyperactivity disorder and autism spectrum disorder.  Abstract:

Nutrition plays an important role in neurodevelopment. This insight has led to increasing research into the efficacy of nutrition-related interventions for treating neurodevelopmental disorders. This review discusses an elimination diet as a treatment for attention deficit hyperactivity disorder and autism spectrum disorder, with a focus on the efficacy of the food additives exclusion diet, gluten-free/casein-free diet and oligoantigenic diet. Furthermore, we discuss the potential mechanisms of elimination diets' effects in these neurodevelopmental disorders. The main candidate mechanism is the microbiome-gut-brain axis possibly involving complex interactions between multiple systems, including the metabolic, immune, endocrine, and neural system. We conclude with practical implications and future directions into the investigation of an elimination diet's efficacy in the treatment of attention deficit hyperactivity disorder and autism spectrum disorder.

Once again we see the power of nutrition and diet to affect serious human health and developmental problems, and we note the mention of "the microbiome-gut-brain axis" - demonstrating, also once again, the relevance of the gut microbiome to various aspects of human well-being.

Additional Studies On Ketogenic Diets And Epilepsy

More information on ketogenic diets, abstract:

PURPOSE OF REVIEW:High-fat, low-carbohydrate ketogenic diets have been used for almost a century for the treatment of epilepsy. Used traditionally for the treatment of refractory pediatric epilepsies, in recent years the use of ketogenic diets has experienced a revival to include the treatment of adulthood epilepsies as well as conditions ranging from autism to chronic pain and cancer. Despite the ability of ketogenic diet therapy to suppress seizures refractory to antiepileptic drugs and reports of lasting seizure freedom, the underlying mechanisms are poorly understood. This review explores new insights into mechanisms mobilized by ketogenic diet therapies.RECENT FINDINGS:Ketogenic diets act through a combination of mechanisms, which are linked to the effects of ketones and glucose restriction, and to interactions with receptors, channels, and metabolic enzymes. Decanoic acid, a component of medium-chain triclycerides, contributes to seizure control through direct α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor inhibition, whereas drugs targeting lactate dehydrogenase reduce seizures through inhibition of a metabolic pathway. Ketogenic diet therapy also affects DNA methylation, a novel epigenetic mechanism of the diet.SUMMARY:Ketogenic diet therapy combines several beneficial mechanisms that provide broad benefits for the treatment of epilepsy with the potential to not only suppress seizures but also to modify the course of the epilepsy.

Epileptic patients may wish to  discuss these findings with their physician to determine whether dietary modifications may be of use in their own case.

Some Adventures In Body Composition

Does body composition affect food intake and, hence, obesity?  It seems so.  Abstract:

In his last review entitled "Some Adventures in Body Composition," Gilbert Forbes reminded us that "lean body mass and body fat are in a sense companions." To what extent the lean body mass (or fat-free mass) component in this companionship impacts on energy intake is rarely a topic for discussion, amid a dominant adipocentric view of appetite control. Yet an analysis of the few human studies that have investigated the relationships between objectively measured food intake and body composition reveals a potentially important role for both an increase and a decrease in fat-free mass in the drive to eat. These studies are highlighted here, together with the implications of their findings for research directed as much toward the elucidation of peripheral signals and energy-sensing mechanisms that drive hunger and appetite, as toward understanding the mechanisms by which dieting and sedentariness predispose to fatness.

A deficit in lean body mass may lead to overeating/obesity, dieting may, and a sedentary lifestyle.  It would seem that exercise that builds lean body mass, overall physical activity, and a healthy diet that avoids overly strict "fad dieting" may all be helpful in regard to this.

Rare Variants For Human Height

At left, genetics of height. By The original uploader was Pete.Hurd at English Wikipedia - Transferred from en.wikipedia to Commons by MichaelSchoenitzer using CommonsHelper., Public Domain, 

https://commons.wikimedia.org/w/index.php?curid=19496489

Interesting paper, abstract:

Height is a highly heritable, classic polygenic trait with approximately 700 common associated variants identified through genome-wide association studies so far. Here, we report 83 height-associated coding variants with lower minor-allele frequencies (in the range of 0.1-4.8%) and effects of up to 2 centimetres per allele (such as those in IHH, STC2, AR and CRISPLD2), greater than ten times the average effect of common variants. In functional follow-up studies, rare height-increasing alleles of STC2 (giving an increase of 1-2 centimetres per allele) compromised proteolytic inhibition of PAPP-A and increased cleavage of IGFBP-4 in vitro, resulting in higher bioavailability of insulin-like growth factors. These 83 height-associated variants overlap genes that are mutated in monogenic growth disorders and highlight new biological candidates (such as ADAMTS3, IL11RA and NOX4) and pathways (such as proteoglycan and glycosaminoglycan synthesis) involved in growth. Our results demonstrate that sufficiently large sample sizes can uncover rare and low-frequency variants of moderate-to-large effect associated with polygenic human phenotypes, and that these variants implicate relevant genes and pathways.

Obviously, there's nothing you can do about what gene variants you inherited and nothing you can do about height as an adult, but genetic height potential can be maximized by having adequate nutrition while growing, which is why people in given populations tend to be taller today than in centuries past.

Dietary Interventions For Sarcopenia

Sarcopenia is the loss of muscle with normal aging.  What dietary interventions can help improve muscle mass in these patients?  Abstract:

BACKGROUND: Inadequate nutritional intake and altered response of aging muscles to anabolic stimuli from nutrients contribute to the development of sarcopenia. Nutritional interventions show inconsistent results in sarcopenic older adults, which might be influenced by their basal nutritional status.

OBJECTIVE: To test if baseline serum 25-hydroxyvitamin D (25(OH)D) concentrations and dietary protein intake influenced changes in muscle mass and function in older adults who received nutritional intervention.

METHODS AND DESIGN: Post-hoc analysis was performed in the PROVIDE study that was a randomized controlled, double blind trial among 380 sarcopenic older adults. This study showed that those who received a vitamin D and leucine-enriched whey protein medical nutrition drink for 13 weeks gained more appendicular muscle mass (aMM), and improved lower-extremity function as assessed by the chair stand test compared with controls. To define low and high groups, a baseline serum concentration of 50 nmol/L 25(OH)D and baseline dietary protein intake of 1.0 g/kg/d were used as cut offs.

RESULTS: At baseline, participants with lower 25(OH)D concentrations showed lower muscle mass, strength and function compared with participants with a high 25(OH)D, while the group with lower protein intake (g/kg/day) had more muscle mass at baseline compared with the participants with higher protein intake. Participants with higher baseline 25(OH)D concentrations and dietary protein intake had, independent of other determinants, greater gain in appendicular muscle mass, skeletal muscle index (aMM/h2), and relative appendicular muscle mass (aMM/body weight × 100%) in response to the nutritional intervention. There was no effect modification of baseline 25(OH)D status or protein intake on change in chair-stand test.

CONCLUSIONS: Sufficient baseline levels of 25(OH)D and protein intake may be required to increase muscle mass as a result of intervention with a vitamin D and protein supplement in sarcopenic older adults. This suggests that current cut-offs in the recommendations for vitamin D and protein intake could be considered the "minimum" for adults with sarcopenia to respond adequately to nutrition strategies aimed at attenuating muscle loss.

It may not be surprising that patients with higher baseline vitamin D and protein intake showed greater muscle gains when given the enriched drink intervention.  It is curious that at baseline, while the higher vitamin D intake group had greater muscle mass, it was the lower protein intake group that had greater muscle mass.  The higher protein intake group had more women that the lower group, less weight and less fat, so there are a number of factors to consider.  The bottom line though is that gain of muscle above baseline required sufficient vitamin D and protein.