Phyiscal Activity and Pregnancy

First article looked at today concludes:

This meta-analysis suggests that higher leisure-time activity is associated with reduced risk of preterm birth. 

So, there is a possibility that a certain degree of physical activity reduces the chances that the mother will have  a preterm birth.  

What about gestational diabetes?  See here, abstract:

Physical activity has been inconsistently associated with risk of gestational diabetes mellitus in epidemiological studies, and questions remain about the strength and shape of the dose-response relationship between the two. We therefore conducted a systematic review and meta-analysis of cohort studies and randomized trials on physical activity and gestational diabetes mellitus. PubMed, Embase and Ovid databases were searched for cohort studies, and randomized controlled trials of physical activity and risk of gestational diabetes mellitus, up to August 5th 2015. Summary relative risks (RRs) were estimated using a random effects model. Twenty-five studies (26 publications) were included. For total physical activity the summary RR for high versus low activity was 0.62 (95 % CI 0.41-0.94, I2 = 0 %, n = 4) before pregnancy, and 0.66 (95 % CI 0.36-1.21, I2 = 0 %, n = 3) during pregnancy. For leisure-time physical activity the respective summary RRs for high versus low activity was 0.78 (95 % CI 0.61-1.00, I2 = 47 %, n = 8) before pregnancy, and it was 0.80 (95 % CI 0.64-1.00, I2 = 17 %, n = 17) during pregnancy. The summary RR for pre-pregnancy activity was 0.70 (95 % CI 0.49-1.01, I2 = 72.6 %, n = 3) per increment of 5 h/week and for activity during pregnancy was 0.98 (95 % CI 0.87-1.09, I2 = 0 %, n = 3) per 5 h/week. There was evidence of a nonlinear association between physical activity before pregnancy and the risk of gestational diabetes mellitus, pnonlinearity = 0.005, with a slightly steeper association at lower levels of activity although further reductions in risk were observed up to 10 h/week. There was also evidence of nonlinearity for physical activity in early pregnancy, pnonlinearity = 0.008, with no further reduction in risk above 8 h/week. There was some indication of inverse associations between walking (before and during pregnancy) and vigorous activity (before pregnancy) and the risk of gestational diabetes mellitus. This meta-analysis suggests that there is a significant inverse association between physical activity before pregnancy and in early pregnancy and the risk of gestational diabetes mellitus. Further studies are needed to clarify the association between specific types and intensities of activity and gestational diabetes mellitus.

So it seems physical activity can be helpful there as well. Of course, for both articles, this is for the general population; there may be individual cases where physical activity is restricted during pregnancy for health reasons.  

Sedentary Lifestyle And Your RNA

Take a look at this paper from several years ago, abstract:

Pioneering epidemiological work has established strong association of sedentary lifestyle and obesity with the risk of colorectal cancer, while the detailed underlying mechanism remains unknown. Here we show that Hotair (HOX transcript antisense RNA) is a pro-adipogenic long non-coding RNA highly expressed in gluteal-femoral fat over other fat depots. Hotair knockout in adipose tissue results in gluteal-femoral fat defect. Squeeze of the gluteal-femoral fat induces intestinal proliferation in wildtype mice, while not in Hotair knockout mice. Mechanistically, squeeze of the gluteal-femoral fat induces exosomal Hotair secretion mainly by transcriptional upregulation of Hotair via NFκB. And increased exosomal Hotair in turn circulates in the blood and is partially endocytosed by the intestine, finally promoting the stemness and proliferation of intestinal stem/progenitor cells via Wnt activation. Clinically, obese subjects with sedentary lifestyle have much higher exosomal HOTAIR expression in the serum. These findings establish that sedentary lifestyle promotes exosomal Hotair release from the gluteal-femoral fat, which in turn facilitates intestinal stem and/or progenitor proliferation, raising a possible link between sedentary lifestyle with colorectal tumorigenesis.

So, there is a link between a sedentary lifestyle, and release of this HOTAIR RNA from fat, which in turn promotes the growth of intestinal stem cells and/or progenitors - cells that form the target population for mutation leading to colorectal cancer.  The importance of an active lifestyle and a lean physique is underscored by these findings, in my opinion.

Myoststin Knockout Improves Cachexia And Inhibits Tumor Growth

Cachexia- induced muscle wasting is a problem in cancer. This paper tests the hypothesis that knocking out myostatin expression could help with this problem, since myostatin inhibits muscle growth and differentiation.  In mice, this hypothesis proved correct and also some inhibition of tumor growth was also observed - these are all encouraging findings.  The abstract of the paper:

Cachexia is a muscle-wasting syndrome that contributes significantly to morbidity and mortality of many patients with advanced cancers. However, little is understood about how the severe loss of skeletal muscle characterizing this condition occurs. In the current study, we tested the hypothesis that the muscle protein myostatin is involved in mediating the pathogenesis of cachexia-induced muscle wasting in tumor-bearing mice. Myostatin gene inactivation prevented the severe loss of skeletal muscle mass induced in mice engrafted with Lewis lung carcinoma (LLC) cells or in Apc(Min) (/+) mice, an established model of colorectal cancer and cachexia. Mechanistically, myostatin loss attenuated the activation of muscle fiber proteolytic pathways by inhibiting the expression of atrophy-related genes, MuRF1 and MAFbx/Atrogin-1, along with autophagy-related genes. Notably, myostatin loss also impeded the growth of LLC tumors, the number and the size of intestinal polyps in Apc(Min) (/+) mice, thus strongly increasing survival in both models. Gene expression analysis in the LLC model showed this phenotype to be associated with reduced expression of genes involved in tumor metabolism, activin signaling, and apoptosis. Taken together, our results reveal an essential role for myostatin in the pathogenesis of cancer cachexia and link this condition to tumor growth, with implications for furthering understanding of cancer as a systemic disease.

More research is needed.

Identifying And Targeting Cancer Stem Cells

Here is a paper from several years ago demonstrating further identification of (colon) cancer stem cells, with information on targeting such cells for therapy.  Abstract:

The cancer stem cell (CSC) theory highlights a self-renewing subpopulation of cancer cells that fuels tumour growth. The existence of human CSCs is mainly supported by xeno-transplantation of prospectively isolated cells, but their clonal dynamics and plasticity remain elusive. Here, we demonstrate that human LGR5+ colorectal cancer cells serve as CSCs in growing cancer tissues. Lineage-tracing experiments with a CRISPR-Cas9-mediated LGR5-CreER knock-in allele reveal self-renewal and differentiation capacity of LGR5+ tumour cells. Selective ablation of LGR5+ CSCs in LGR5-iCaspase9 knock-in organoids leads to tumour regression, followed by tumour regrowth driven by re-emerging LGR5+ CSCs. KRT20-CreER marks differentiated cancer cells that constantly diminish in tumour tissues, while reverting to LGR5+ CSCs and contributing to tumour regrowth after LGR5+ CSC ablation. We also show that combined chemotherapy potentiates LGR5+ CSCs targeting. These data provide insights into the plasticity of CSCs and their potential as a therapeutic target in human colorectal cancer.

We'll be following further developments in this field.

Targeting Senescent Cells

Here is a paper from several years ago suggesting that targeting senescent cells with programmed cell death can reverse aspects of aging in mice.  Older studies suggested rapamycin or carnosine as anti-aging interventions. We will be keeping track of further developments in this field.

Yet Another Reason Not To Smoke

Tobacco pipes and car airbags don't mix, abstract:

Airbags have been shown to reduce injuries and save the lives of car occupants in a crash. Like any protection system, airbags potentially introduce some new risks if no appropriate countermeasures are taken. A case of a relatively moderate frontal impact is described where the driver of an airbag-equipped car suffered a severe penetrating eye injury after the airbag deployed. Since the airbag fabric itself was excluded as an injury-producing structure, other objects such as eyeglasses, a wrist-watch, a bracelet, and a large finger ring had to be assessed. The investigation of the car interior as well as the morphologic details of the injuries to the eye and the face revealed that the most likely candidate for the injury was a tobacco pipe, which was probably being held in one hand and was broken apart by the deploying airbag and projected into the face of the driver. This case illustrates the hazard of having any rigid object between the occupant and the deploying airbag. The desirability of warning car occupants of the potential hazards which can result from today's protection systems is also discussed.

Don't smoke.

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.

Age And Triathlon Performance

How does Ironman triathlon performance change with age?  Abstract:

In Ironman triathlon, the number of overall male and female finishers increased in the last 30 years, while an improvement in performance has been reported. Studies concluding these numbers only analysed the top ten athletes per age group instead of all finishers, therefore a selection bias might have occurred. The aim of the present study was to investigate participation, performance and the age-related performance decline of all pro and age group triathletes ranked in all Ironman triathlons held worldwide between 2002 and 2015. Split and overall race times of 329,066 (80%) male and 81,815 (20%) female athletes competing in 253 different Ironman triathlon races were analysed. The number of finishers increased in all age groups with exception of women in age group 75-79 years. In pro athletes, performance improved in all disciplines. In age group athletes, performance improved in younger age groups for running (18-24 to 40-44 years) and older age groups for swimming (50-54 to 65-69 years) and cycling (35-39 to 55-59 years), while it impaired in younger age groups for swimming (18-24 to 45-49 years) and cycling (18-24 to 30-34), and older age groups in running (45-49 to 70-74 years). The age-related performance decline started in women in age group 25-29 years in swimming and in age group 30-34 years in cycling, running and overall race time, whereas it started in men in age group 25-29 years in swimming and in age group 35-39 years in cycling, running and overall race time. For athletes and coaches, performance improved in younger age groups for running and older age groups for swimming and cycling and the age-related decline in performance started earlier in swimming than in cycling and running. In summary, women should start competing in Ironman triathlon before the age of 30 years and men before the age of 35 years to achieve their personal best Ironman race time.

It is interesting that performance in swimming declined earlier with age than in cycling and running, suggesting that swimming is the most intense exercise of the three.  The last sentence suggests that Ironman  is best for the young.

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.

Carbs And Protein For Muscle Recovery

A paper from several years ago supports the traditional wisdom for post-workout muscle recover, abstract:

The objective of the study was to investigate whether co-ingestion of carbohydrate and protein as compared with protein alone augments muscle protein synthesis (MPS) during early exercise recovery. Two months old rats performed 10 repetitions of ladder climbing with 75% of body weight attached to their tails. Placebo (PLA), whey protein (WP), or whey protein plus carbohydrate (CP) was then given to rats by gavage. An additional group of sedentary rats (SED) was used as controls. Blood samples were collected immediately and at either 1 or 2 h after exercise. The flexor hallucis longus muscle was excised at 1 or 2 h post exercise for analysis of MPS and related signaling proteins. MPS was significantly increased by CP compared with PLA (p<0.05), and approached significance compared with WP at 1 h post exercise (p = 0.08). CP yielded a greater phosphorylation of mTOR compared with SED and PLA at 1 h post exercise and SED and WP at 2 h post exercise. CP also increased phosphorylation of p70S6K compared with SED at 1 and 2 h post exercise. 4E-BP1 phosphorylation was inhibited by PLA at 1 h but elevated by WP and CP at 2 h post exercise relative to SED. The phosphorylation of AMPK was elevated by exercise at 1 h post exercise, and this elevated level was sustained only in the WP group at 2 h. The phosphorylation of Akt, GSK3, and eIF2Bε were unchanged by treatments. Plasma insulin was transiently increased by CP at 1 h post exercise. In conclusion, post-exercise CP supplementation increases MPS post exercise relative to PLA and possibly WP, which may have been mediated by greater activation of the mTOR signaling pathway

Carbs and protein post-resistance training therefore proved here superior to protein alone.