Legumes And Colorectal Adenoma Risk

An unsurprising finding is that legume consumption is associated with deceased risk for colorectal adenoma.  More investigations are required because such “meta-analysis” can have confounding variables.  Still, the conclusion is consistent with all else we know about dietary recommendations regarding colorectal cancer prevention. Prevent the adenoma (poly), prevent the carcinoma (cancer). Fiber helps.  Abstract:

Background

The anticancer effects of legumes have been explored extensively, but evidence from epidemiologic studies on colorectal adenoma is controversial. We performed a meta-analysis to assess these issues.

Methods

A systemic search of several databases was conducted for relevant studies evaluating the relationship between legume intake and adenoma risk, with no language restriction, from January 1, 1966, to April 1, 2013.

Results

Three cohort and eleven case control studies with 8,380 cases and a total of 101,856 participants were included in the analysis; the pooled odds ratio (95% confidence interval) for the highest vs. lowest consumption categories was 0.83 (0.75–0.93), with moderate level of heterogeneity (I2 = 25.9% and P = 0.146) based on a random effects model. A decreased risk of adenoma was also observed in most of our subgroup meta-analyses.

Conclusions

Higher intake of legumes significantly reduced the risk of colorectal adenoma in our meta-analysis. Nevertheless, due to possible confounders and bias, further investigations are warranted to confirm this relationship.

Low Carb Ironman Training?

One possible way to overcome carbohydrate (carb) storage limitations for extreme duration athletic events like Ironman triathlons is for the athlete to train under a low-carb diet, to get the body acclimated to that condition, and then giving carb supplementation during the completion, providing the levels that the now-adjusted body can utilize.  Keep in mind that another study, looking at elite race walkers (somewhat less extreme that the Ironman) found that low carb diets were negative for performance.  So the current finding (abstract below) may apply only to the most extreme events where “carb loading is inefficient?  More study is required.

Ironman triathlons are ultra-endurance events of extreme duration. The performance level of those competing varies dramatically, with elite competitors finishing in ~ 8:00:00, and lower performing amateurs finishing in ~ 14-15:00:00. When applying appropriate values for swimming, cycling and running economies to these performance times, it is demonstrated that the absolute energy cost of these events is high, and the rate of energy expenditure increases in proportion with the athlete's competitive level. Given the finite human capacity for endogenous carbohydrate storage, minimising the endogenous carbohydrate cost associated with performing exercise at competitive intensities should be a goal of Ironman preparation. A range of strategies exist that may help to achieve this goal, including, but not limited to, adoption of a low-carbohydrate diet, exogenous carbohydrate supplementation and periodised training with low carbohydrate availability. Given the diverse metabolic stimuli evoked by Ironman triathlons at different performance levels, it is proposed that the performance level of the Ironman triathlete is considered when adopting metabolic strategies to minimise the endogenous carbohydrate cost associated with exercise at competitive intensities. Specifically, periodised training with low carbohydrate availability combined with exogenous carbohydrate supplementation during competition might be most appropriate for elite and top-amateur Ironman triathletes who elicit very high rates of energy expenditure. Conversely, the adoption of a low-carbohydrate or ketogenic diet might be appropriate for some lower performance amateurs (> 12 h), in whom associated high rates of fat oxidation may be almost completely sufficient to match the energy demands required.

Muscle Damage Not Required For Muscle Growth In Resistance Training?

Muscle growth die to resistance may not be dependent on muscle damage (and subsequent repair of that damage) induced by training. If true, this is contrary to the paradigm of bodybuilding.  Abstract:

Resistance training (RT)-induced skeletal muscle hypertrophy is a highly intricate process. Despite substantial advances, we are far from understanding exactly how muscle hypertrophy develops during RT. The aim of the present review is to discuss new insights related to the role of skeletal muscle damage and muscle protein synthesis (MPS) in mediating RT-induced hypertrophy. Specifically, the thesis that in the early phase of RT (≤ 4 previous RT sessions) increases in muscle cross-sectional area are mostly attributable to muscle damage-induced muscle swelling; then (after ~ 10 sessions), a modest magnitude of muscle hypertrophy ensues; but only during a latter phase of RT (after ~ 18 sessions) is true muscle hypertrophy observed. We argue that the initial increases in MPS post-RT are likely directed to muscle repair and remodelling due to damage, and do not correlate with eventual muscle hypertrophy induced by several RT weeks. Increases in MPS post-RT session only contribute to muscle hypertrophy after a progressive attenuation of muscle damage, and even more significantly when damage is minimal. Furthermore, RT protocols that do not promote significant muscle damage still induce similar muscle hypertrophy and strength gains compared to conditions that do promote initial muscle damage. Thus, we conclude that muscle damage is not the process that mediates or potentiates RT-induced muscle hypertrophy.

Newstart Lifestyle?

The Newstart Lifestyle program claims the ability to lower blood pressure as effectively as medication.  In general, I approve of such approaches’ it is good if physicians and patients use medication as a last resort instead of a first-line treatment.  I quibble with some details; for example, I doubt that a strictly vegan diet is really necessary, not desirable for optimal health.  As regards the “spiritual activities” at least they are deemed “optional” – if that was required I would more strongly object.  In my case I lowered blood pressure by: losing abdominal fat (“spare tire”), reducing saturated fat and excess sugar, eating more fruit, and getting more aerobic exercise mostly in the form of walking with some occasional brief jumping rope thrown in several days per week.

June 11 (UPI) -- By modifying their lifestyle, including diet and exercise, people can lower their blood pressure just as effectively as with medication, according to a study.

Researchers studied the effects of adapting the Newstart Lifestyle program, which includes a vegan diet, daily outside walks, substantial quantities of water, adequate daily sleep and optional spiritual activities. The findings will be presented Monday at the American Society for Nutrition's annual meeting, Nutrition 2018, in Boston.

The idea of altering diet as part of treatment for high blood pressure is not a new one -- most people with hypertension, among other cardiovascular conditions, are advised to change their diet, and often also to get some exercise.

A study published in the Journal of the American College of Cardiology in 2017 also found that a low-salt and heart-healthy diet may be just as effective as medication. The diet for that study, called the Dietary Approaches to Stop Hypertension, or DASH, has been endorsed by the American Heart Association.

The latest research involved the Newstart program of lifestyle changes.

"The Newstart Lifestyle program works quickly, is inexpensive and uses a palatable diet that allows for moderate amounts of salt and healthy fats from nuts, olives, avocado and certain vegetable oils," M. Alfredo Mejia, an associate professor at Andrews University in Berrien Springs, Mich., said in a press release.

On its website, Newstart touts that half of all hypertensives are off medication and return to normal blood pressure. Also, 50 percent of type 2 diabetics who adopt the system are off insulin and medications in as little as 18 days.

The website includes testimonials from people getting off medication.

The researchers' study confirmed the results. They found half of people in the study achieved normal blood pressure --- the recommended 120 mmHg -- within two weeks and avoided the side effects and costs of blood pressure medications, despite lowering their blood pressure on average 14 percent.

Researchers evaluated data from 117 people with high blood pressure who had participated in the Newstart Lifestyle program at the Weimer Institute in California for 16 days in 2014. Their average age was 66.5 years old with a body mass index of 31.6 and blood pressure of 138 mmHg.

Blood pressure was lower in people who have several medical conditions but are healthy otherwise -- women and people with diabetes, who are obese or have high cholesterol levels.

The researchers plan to expand studies of the program to more people, and over a longer time period. They also want to see if the diet improves other health problems, including diabetes, cardiovascular disease and obesity.

The Mayo Clinic offers a set of lifestyle changes that can lower blood pressure and reduce risk of heart disease which are reminiscent to those noted in the new study, as well as in previous research on high blood pressure and diet.

Changes spotlighted by researchers at Mayo include regular exercise, healthy diet, limiting alcohol, smoking cessation, reduces caffeine and sodium and lower stress.

"If you successfully control your blood pressure with a healthy lifestyle, you might avoid, delay or reduce the need for medication," the organization has included in its recommendations.

Inhibiting Hippo For Heart Repair

Altering cell signaling pathways, as discussed here with the Hippo pathway, holds promise to enhance the regenerative capacity of damaged tissues and organs, in this case, the heart, after heart failure. Abstract:

Mammalian organs vary widely in regenerative capacity. Poorly regenerative organs, such as the heart are particularly vulnerable to organ failure. Once established, heart failure commonly results in mortality. The Hippo pathway, a kinase cascade that prevents adult cardiomyocyte proliferation and regeneration, is upregulated in human heart failure. Here we show that deletion of the Hippo pathway component Salvador (Salv) in mouse hearts with established ischaemic heart failure after myocardial infarction induces a reparative genetic program with increased scar border vascularity, reduced fibrosis, and recovery of pumping function compared with controls. Using translating ribosomal affinity purification, we isolate cardiomyocyte-specific translating messenger RNA. Hippo-deficient cardiomyocytes have increased expression of proliferative genes and stress response genes, such as the mitochondrial quality control gene, Park2. Genetic studies indicate that Park2 is essential for heart repair, suggesting a requirement for mitochondrial quality control in regenerating myocardium. Gene therapy with a virus encoding Salv short hairpin RNA improves heart function when delivered at the time of infarct or after ischaemic heart failure following myocardial infarction was established. Our findings indicate that the failing heart has a previously unrecognized reparative capacity involving more than cardiomyocyte renewal.

Cancer Immunotherapy: The Systemic Response

An article  on cancer immunotherapy; the abstract:

Immune responses involve coordination across cell types and tissues. However, studies in cancer immunotherapy have focused heavily on local immune responses in the tumor microenvironment. To investigate immune activity more broadly, we performed an organism-wide study in genetically engineered cancer models using mass cytometry. We analyzed immune responses in several tissues after immunotherapy by developing intuitive models for visualizing single-cell data with statistical inference. Immune activation was evident in the tumor and systemically shortly after effective therapy was administered. However, during tumor rejection, only peripheral immune cells sustained their proliferation. This systemic response was coordinated across tissues and required for tumor eradication in several immunotherapy models. An emergent population of peripheral CD4 T cells conferred protection against new tumors and was significantly expanded in patients responding to immunotherapy. These studies demonstrate the critical impact of systemic immune responses that drive tumor rejection.

In other words, a local response at the tumor by the immune system is sufficient for sustained proliferation of the immune response required for tumor rejection.  A (body-wide) systemic immune response is required, a set of responses that, as the article states "involve coordination across cell types and tissues."

It would stand to reason, as my hypothesis, that those things that would enhance the overall function of the immune system - diet, exercise, proper sleep,  less stress, and possibly the gut microbiota - would assist the body in generating the systemic responses required for tumor rejection.  More studies are required to evaluate my hypothesis.

Have fun in the kitchen!

No, happiness is not in the freezer and the next ice cream container. It is in your health - if you are healthy, there is a good chance that you would be happy. 

Healthy eating can get you out of the doctor's office and off most medications. Start your transformation by committing to several decisions:

I will do healthy food swaps
Take a favorite recipe and transform it into a healthy recipe. When you cook, make your traditional/family recipes “healthy” by substituting ingredients. Or sign up for Pinterest and collect great recipes to experiment with.

I will grill the healthy way
If you do not want to give up red meat, you do not have to. However, the maximum recommended amount of meat a week is 18 ounces. A portion of red meat the size of a deck of cards can be served up to six times a week. Find some great grilling advice here.

I will not eat added sugar 
Be able to recognize the 50 names of sugar: avoid any added sugar; read the nutrition labels and know what NOT to buy.

B: Barley malt, Beet sugar, Brown sugar, Buttered syrup
C: Cane juice crystals, Cane sugar, Caramel, Corn syrup, Corn syrup solids, Confectioner’s sugar, Carob syrup, Castor sugar
D: Date sugar, Demerara sugar, Dextran, Dextrose, Diastatic malt, Diatase
E: Ethyl maltol
F: Fructose, Fruit juice, Fruit juice concentrate
G: Galactose, Glucose, Glucose solids, Golden sugar, Golden syrup, Grape sugar
H: High-fructose corn syrup, Honey
I: Icing sugar, Invert sugar
L: Lactose
M: Maltodextrin, Maltose, Malt syrup, Maple syrup, Molasses, Muscovado sugar
P: Panocha
R: Raw sugar, Refiner’s syrup, Rice syrup
S: Sorbitol, Sorghum syrup, Sucrose, Sugar
T: Treacle, Turbinado sugar 
Y: Yellow sugar  
I will make sure that I have complete protein
Different proteins have different combinations of the building blocks (amino acids). You need to consume proteins of different sources to obtain “complete” source of amino acids. Find sample menu on this website.

More on protein
How much protein do you need? Here is a quick estimate of your protein requirement: Take your weight (in pounds) and divide by 2. The number you get is the approximate number of grams of protein you need daily. Example: If you weigh 180 pounds, 180 ÷ 2 = 90 grams of protein daily. If you are receiving cancer treatment, you may need more protein. A dietitian can help you figure out your protein needs during treatment. This advice and more comes from this website.

Fun recipes
Golden Quick Barley with Sweet Peas and Corn: on this website.
Party time, “Create Your Own Beverage Bar”: on this website.

Drugging Test Anxiety?

I suppose this can be the next grand adventure in “learning disability” pharmaceutical adjustments: taking drugs for “test anxiety.”  At some point people need to be able to get through life without being medicated for every stressful scenario unfolding in their lives.  Abstract:

Test anxiety is severely disabling to students whose fear of examinations causes cognitive dysfunction that paralyzes their thinking the way stage fright impairs actors ability to act. In studies using subjective evaluations among actors and musicians, beta-blockade relieved stage fright and has been used informally to treat test anxiety in students without objective measures of effectiveness. The Scholastic Aptitude Test (SAT) was chosen as an objective test instrument to confirm the effect of beta-blockade on test anxiety and performance. Thirty-two high school students who had already taken the SAT before enrolling in this study and who had stress-induced cognitive dysfunction on exams were given 40 mg of propranolol one hour before they retook those tests. Mean SAT scores with beta-blockade were 130 points higher than on the initial SAT done before entering the study without medication (p = less than .01). A single dose of propranolol immediately before the SAT permitted improved performance in students prone to cognitive dysfunction due to test anxiety.

Repurposing Old Drugs For New Roles

Here is an interesting article about expanding the use of old, approved drugs for new purposes.  In theory, this is a good idea, since the safety profile of the drug and its various side effects would already be known, and sometimes “side effects” can mean the drug can be useful against other disorders than originally intended.  However, this requires additional testing to determine if the drug is actually effective in the new role for which it is being proposed. The problem is that when you consider expensive drugs still under patent, pharmaceutical companies have a patent incentive to do such testing, but not for low-cost generic drugs. The author proposes some ways around this: government funding, prize funds, leveraging existing data.  Given the cost of new drugs and the uncertainty of side effects, particularly long-term side effects, once they are in clinical use, repurposing old drugs has promise in being more safe and efficient.  From the article:

US Food and Drug Administration (FDA) approval of a new drug typically coincides with a period of patent protection, during which the manufacturer will often apply for additional indications to expand the market for the product. For example, the tyrosine kinase inhibitor imatinib (Gleevec; Novartis) was originally approved to treat Philadelphia chromosome–positive chronic myelogenous leukemia, but has since been approved for treatment of other cancers. Many noncancer drugs also follow this pattern, including botulinum toxin A (Botox; Allergan), which was originally approved for the treatment of strabismus and blepharospasm and subsequently approved for treatment of cervical dystonia, cosmetic uses, and chronic migraine.

This pattern of additional testing and approvals is common for more expensive on-patent drugs, but new indications are rarely sought for less-expensive generic drugs, for which it is more difficult to profit from the research. This creates a policy conundrum: follow-on innovation for low-cost generic products offers a rare opportunity to simultaneously improve health outcomes and likely reduce health care expenditures, but how could such research be encouraged?

Against Colitis And Cancer

Chronic inflammation of the colon can increase risk for cancer; an antibody to a pro-inflammatory mediator can reduce inflammation in a mouse model, reducing cancer risk through the modulation of important cancer- related signaling pathways that can be affected by inflammation.  This is a promising therapeutic approach.  Abstract:

The association between chronic inflammation and cancer has long been recognized. The inflammatory bowel disease ulcerative colitis frequently progresses to colon cancer; however, the underlying mechanism is still unclear. S100a9 has been emerged as an important pro-inflammatory mediator in acute and chronic inflammation, and the aberrant expression of S100a9 also contributes to tumorigenic processes such as cell proliferation, angiogenesis, metastasis, and immune evasion. We previously revealed that S100a8 and S100a9 are highly activated and play an important role in the process of colitis-associated carcinogenesis, which suggests an attractive therapeutic target for ulcerative colitis and related colon cancer. Here, we report that administration of a neutralizing anti-S100a9 antibody significantly ameliorated dextran sulfate sodium (DSS)-induced colitis and accompanied by diminished cellular infiltrate of innate immunity cells (macrophages, neutrophils, and dendritic cells) and production of pro-inflammatory cytokines (Tnfα, Il1β, Ifnγ, Il6, Il17a, Il23a, Il4, and Il12a). The protective effect of anti-S100a9 antibody treatment was also observed in azoxymethane (AOM)/DSS-induced colitis-associated cancer (CAC) mouse model. The inflammatory response, tumor cell proliferation, and immune cells infiltration in the colon tissues were suppressed by anti-S100a9 antibody. Gene expression profiling showed that key pathways known to be involved in CAC development, such as Wnt signaling pathway, PI3K-Akt signaling pathway, cytokine-cytokine receptor interaction, and ECM-receptor interaction pathway, were suppressed after treatment with anti-S100a9 antibody in CAC mice. In view of the protective effect of neutralizing anti-S100a9 antibody against DSS-induced colitis and AOM/DSS-induced CAC in mouse model, this study suggests that anti-S100a9 antibody may provide a novel therapeutic approach to treat ulcerative colitis and may decrease the risk for developing CAC.