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.

Resistance Training And Muscle Metabolism

Here is a paper from several years ago formally demonstrating what bodybuilders have long put into practice: resistance training affects protein turnover in skeletal muscle so as to result in muscle growth.  Abstract:

PURPOSE:

Acute bouts of resistance exercise and subsequent training alters protein turnover in skeletal muscle. The mechanisms responsible for the changes in basal post-absorptive protein turnover and its impact on muscle hypertrophy following resistance exercise training are unknown. Our goal was to determine whether post-absorptive muscle protein turnover following 12 weeks of resistance exercise training (RET) plays a role in muscle hypertrophy. In addition, we were interested in determining potential molecular mechanisms responsible for altering post-training muscle protein turnover.

METHODS:

Healthy young men (n = 31) participated in supervised whole body progressive RET at 60-80% 1 repetition maximum (1-RM), 3 days/week for 3 months. Pre- and post-training vastus lateralis muscle biopsies and blood samples taken during an infusion of 13C6 and 15N phenylalanine and were used to assess skeletal muscle protein turnover in the post-absorptive state. Lean body mass (LBM), muscle strength (determined by dynamometry), vastus lateralis muscle thickness (MT), myofiber type-specific cross-sectional area (CSA), and mRNA were assessed pre- and post-RET.

RESULTS:

RET increased strength (12-40%), LBM (~5%), MT (~15%) and myofiber CSA (~20%) (p < 0.05). Muscle protein synthesis (MPS) increased 24% while muscle protein breakdown (MPB) decreased 21%, respectively. These changes in protein turnover resulted in an improved net muscle protein balance in the basal state following RET. Further, the change in basal MPS is positively associated (r = 0.555, p = 0.003) with the change in muscle thickness.

CONCLUSION:

Post-absorptive muscle protein turnover is associated with muscle hypertrophy during resistance exercise training.

It is always comforting when science supports popular conception.

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.

Gene Therapy For Sickle Cell Disease

Here is a paper from several years ago, abstract:

Sickle cell disease results from a homozygous missense mutation in the β-globin gene that causes polymerization of hemoglobin S. Gene therapy for patients with this disorder is complicated by the complex cellular abnormalities and challenges in achieving effective, persistent inhibition of polymerization of hemoglobin S. We describe our first patient treated with lentiviral vector-mediated addition of an antisickling β-globin gene into autologous hematopoietic stem cells. Adverse events were consistent with busulfan conditioning. Fifteen months after treatment, the level of therapeutic antisickling β-globin remained high (approximately 50% of β-like-globin chains) without recurrence of sickle crises and with correction of the biologic hallmarks of the disease. (Funded by Bluebird Bio and others; HGB-205 ClinicalTrials.gov number, NCT02151526 .).

So, fifteen months of continued therapeutic benefit was observed.  That's very good and stable for that time period. We'll need to look into, and follow up on, continuing developments in this field; but in general, gene therapy opens up exciting avenues of novel therapeutics to treat a variety of inherited and sporadic disorders.

MicroRNA Biomarkers for Type I Diabetes

Here is a paper from several years ago suggesting that circulating microRNAs (small RNA molecules that affect gene expression) can be used to "predict and diagnose" type I diabetes before clinical symptoms are present.  Abstract:

Type 1 diabetes (T1D) is an autoimmune disease that is clinically silent until the majority of β cells are destroyed. There is an unmet need for reliable and cost-effective biomarkers to predict and diagnose diabetes at an early stage. A number of stable microRNAs (miRNAs) have been reported in serum and plasma and are now being investigated as biomarkers of different diseases. We measured the levels of 745 miRNAs in sera of children with recent-onset T1D and age-matched controls using locked nucleic acid-enhanced (LNA-enhanced) quantitative PCR profiling. Thirty-five miRNAs were significantly different between the groups, and 27 miRNAs were elevated in T1D. Good discriminating power was obtained for 6 miRNAs (miR-454-3p, miR-222-3p, miR-144-5p, miR-345-5p, miR-24-3p, and miR-140-5p), which were not elevated at later stages of diabetes. In silico pathway analysis, based on inferred miRNA target genes, associated glycosaminoglycan biosynthesis as well as PI3K/Akt, MAPK, and Wnt signaling pathways with early stages of T1D. Among the 27 upregulated miRNAs in T1D, 2 miRNAs significantly correlated with hemoglobin A1c (HbA1c), as did 5 of 8 downregulated miRNAs. A total of 134 miRNAs significantly correlated with HbA1c when stratifying hyperglycemia-induced miRNAs from T1D-specific miRNAs. In conclusion, we have identified a serum miRNA pattern of recent-onset T1D and signaling pathways that may be involved in its pathogenesis.

The same principle can apply for early diagnosis of other disorders, and we'll be looking at any progress (if any) made since this article came out.  Note also that study of microRNAs is not only useful for identifying biomarkers but also for identifying the cell signaling that is aberrant in disease (as the end of the abstract suggests), leading the way to possible novel therapies.

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.

A Cold Of The Soul

In Japan, like the USA, pharmaceutical companies push over-medication.  See this article, abstract:

In Japan, depression provides the most drastic example of the impact of disease awareness campaigns. Until the late 1990 s, the public's attitude toward depression was generally unfavorable, due to the negative connotations of the Japanese word for clinical depression, 'utsubyou'. After the 1999 introduction of the first selective serotonin re-uptake inhibitor, pharmaceutical companies initiated educational campaigns. In order to aid the drug's acceptance, they coined the catchphrase 'kokoro no kaze', which literally means 'a cold of the soul'. Thanks to these marketing practices, antidepressant sales have increased six fold, from ¥ 14.5 billion in 1998 to ¥ 87 billion in 2006. However, the catchphrase 'kokoro no kaze' masked a critical difference between a cold and depression. It falsified the nature of treatment for depression by concealing the putative duration of medication. Owing to this distortion of information, pharmaceutical companies were assured a steady stream of profits. Now, the pharmaceutical industry is shifting its focus from depression to bipolar disorder. Japanese psychiatrists can learn a great deal from their experience with the aggressive marketing of antidepressants. In the case of depression, over-medication arguably did more harm than good. The same risk exists with other conditions, including bipolar disorder.

Sound familiar?  Now, if medication is necessary, take it.  I do.  But take medication that is necessary, as determined by your physician, your own research, and the cooperation between yourself and your health care team. Talk to your physician, and do research.  Medication solely to boost pharmaceutical profits is not the way to go.  Good medications are saviors, antibiotics have saved millions of lives, and we should not reject biomedical advances.  But the Japanese case outlined here describe a case where unnecessary overmedication has taken place.  One must understand the difference.