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.

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.

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.

Short Chain Fatty Acids And Weight Loss

Can short chain fatty acids contribute to weight loss?  A paper looks at this, abstract:

Elucidating the mechanisms by which short chain fatty acids (SCFA) reduce body weight may assist in the development of an effective weight control strategy. Dietary supplementation of acetate, propionate, butyrate or their admixture was shown to significantly inhibit the body weight gain induced by high-fat diet feeding. Supplementation of SCFAs caused significant changes in the expressions of G-protein coupled receptor 43 (GPR43) and GPR41 characterized by increases in the adipose tissue and reductions in the colon. Additionally, they influenced the bacterial community structure in feces, with a reduction in the proportion of Firmicutes and an increase in the proportion of Bacteroidetes. The effects of dietary SCFAs on the GPR expression and gut microbiota composition may further result in body weight reduction by enhancing triglyceride hydrolysis and FFA oxidation in the adipose tissue, promoting beige adipogenesis and mitochondrial biogenesis, and inhibiting chronic inflammation.

Keep in mind that short chain fatty acids can be produced in the colon by the fermentation of dietary fiber by the gut microbiota, with beneficial effects for colonic health.  However, the effects described in this paper required direct supplementation of these agents into the diet of the test mice.  Nevertheless, the findings suggest a role for short chain fatty acids in weight control.

More Evidence That Nuts Are Good For You

Cardiovascular disease was inhibited to a greater degree by a Mediterranean diet supplemented by olive oil or nuts compared to a control low fat diet.  Abstract:

Background Observational cohort studies and a secondary prevention trial have shown inverse associations between adherence to the Mediterranean diet and cardiovascular risk. Methods In a multicenter trial in Spain, we assigned 7447 participants (55 to 80 years of age, 57% women) who were at high cardiovascular risk, but with no cardiovascular disease at enrollment, to one of three diets: a Mediterranean diet supplemented with extra-virgin olive oil, a Mediterranean diet supplemented with mixed nuts, or a control diet (advice to reduce dietary fat). Participants received quarterly educational sessions and, depending on group assignment, free provision of extra-virgin olive oil, mixed nuts, or small nonfood gifts. The primary end point was a major cardiovascular event (myocardial infarction, stroke, or death from cardiovascular causes). After a median follow-up of 4.8 years, the trial was stopped on the basis of a prespecified interim analysis. In 2013, we reported the results for the primary end point in the Journal. We subsequently identified protocol deviations, including enrollment of household members without randomization, assignment to a study group without randomization of some participants at 1 of 11 study sites, and apparent inconsistent use of randomization tables at another site. We have withdrawn our previously published report and now report revised effect estimates based on analyses that do not rely exclusively on the assumption that all the participants were randomly assigned. Results A primary end-point event occurred in 288 participants; there were 96 events in the group assigned to a Mediterranean diet with extra-virgin olive oil (3.8%), 83 in the group assigned to a Mediterranean diet with nuts (3.4%), and 109 in the control group (4.4%). In the intention-to-treat analysis including all the participants and adjusting for baseline characteristics and propensity scores, the hazard ratio was 0.69 (95% confidence interval [CI], 0.53 to 0.91) for a Mediterranean diet with extra-virgin olive oil and 0.72 (95% CI, 0.54 to 0.95) for a Mediterranean diet with nuts, as compared with the control diet. Results were similar after the omission of 1588 participants whose study-group assignments were known or suspected to have departed from the protocol. Conclusions In this study involving persons at high cardiovascular risk, the incidence of major cardiovascular events was lower among those assigned to a Mediterranean diet supplemented with extra-virgin olive oil or nuts than among those assigned to a reduced-fat diet. (Funded by Instituto de Salud Carlos III, Spanish Ministry of Health, and others; Current Controlled Trials number, ISRCTN35739639 .).

Cancer Stem Cells And Lipid Metabolism

Cancer stem cells seem to have an increased reliance on lipid metabolism, which can be a target for anti-cancer therapy.  I wonder if this has any implications for a ketogenic (high-fat) diet for cancer?  On the one hand, most cancer cells seem “glucose-addicted” so a low-carb, high-fat diet may be preferable.  On the other hand, if cancer stem cells rely more on fat, then will increased dietary fat be a problem?  This question needs to be investigated.  Abstract:

BACKGROUND:

Cancer stem cells (CSCs) or tumor-initiating cells (TICs) represent a small population of cancer cells with self-renewal and tumor-initiating properties. Unlike the bulk of tumor cells, CSCs or TICs are refractory to traditional therapy and are responsible for relapse or disease recurrence in cancer patients. Stem cells have distinct metabolic properties compared to differentiated cells, and metabolic rewiring contributes to self-renewal and stemness maintenance in CSCs.

MAIN BODY:

Recent advances in metabolomic detection, particularly in hyperspectral-stimulated raman scattering microscopy, have expanded our knowledge of the contribution of lipid metabolism to the generation and maintenance of CSCs. Alterations in lipid uptake, de novo lipogenesis, lipid droplets, lipid desaturation, and fatty acid oxidation are all clearly implicated in CSCs regulation. Alterations on lipid metabolism not only satisfies the energy demands and biomass production of CSCs, but also contributes to the activation of several important oncogenic signaling pathways, including Wnt/β-catenin and Hippo/YAP signaling. In this review, we summarize the current progress in this attractive field and describe some recent therapeutic agents specifically targeting CSCs based on their modulation of lipid metabolism.

CONCLUSION:

Increased reliance on lipid metabolism makes it a promising therapeutic strategy to eliminate CSCs. Targeting key players of fatty acids metabolism shows promising to anti-CSCs and tumor prevention effects.

The Taste Of Fats

There does not seem to be a significant genetic component to fat taste sensitivity in humans; abstract:

BACKGROUND:

Individuals with impaired fat taste (FT) sensitivity have reduced satiety responses after consuming fatty foods, leading to increased dietary fat intake. Habitual consumption of dietary fat may modulate sensitivity to FT, with high consumption decreasing sensitivity [increasing fatty acid taste threshold (FATT)] and low consumption increasing sensitivity (decreasing FATT). However, some individuals may be less susceptible to diet-mediated changes in FATT due to variations in gene expression.

OBJECTIVE:

The objective of this study was to determine the effect of an 8-wk low-fat or high-fat diet on FATT while maintaining baseline weight (<2.0 kg variation) to assess heritability and to explore the effect of genetics on diet-mediated changes in FATT.

DESIGN:

A co-twin randomized controlled trial including 44 pairs (mean ± SD age: 43.7 ± 15.4 y; 34 monozygotic, 10 dizygotic; 33 women, 10 men, 1 gender-discordant) was conducted. Twins within a pair were randomly allocated to an 8-wk low-fat (<20% of energy from fat) or high-fat (>35% of energy from fat) diet. FATT was assessed by a 3-alternate forced choice methodology and transformed to an ordinal scale (FT rank) at baseline and at 4 and 8 wk. Linear mixed models were fit to assess diet effect on FT rank and diet effect modification due to zygosity. A variance components model was fit to calculate baseline heritability.

RESULTS:

There was a significant time × diet interaction for FT rank after the 8-wk trial (P < 0.001), with the same conclusions for the subset of participants maintaining baseline weight (low-fat; n = 32; high-fat: n = 35). There was no evidence of zygosity effect modification (interaction of time × diet × zygosity: P = 0.892). Heritability of baseline FT rank was 8%.

CONCLUSIONS:

There appears to be little to no genetic contribution on heritability of FATT or diet-mediated changes to FATT. Rather, environment, specifically dietary fat intake, is the main influencer of FT sensitivity, regardless of body weight. This trial was registered with the Australian New Zealand Clinical Trials Registry at http://www.anzctr.org.au/ as ACTRN12613000466741.

Related: salt promotes passive overconsumption of dietary fat in humans.

Take home point: eating more salt and fat will likely lead to even more fat consumption.

Reducing Inflammation To Combat Cardiovascular Disease

By Transferred from en.wikipedia to Commons., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=2816579

Typically, cardiovascular disease is approached by reducing lipid levels (doctors usually prescribe medication, although dietary changes, and exercise, in our opinion should be focused more on). However, reducing inflammation can reduce the risk of cardiovascular disease independent of lowering lipid levels.  This is an important approach that expands the therapeutic toolkit against cardiovascular disease and underscores the importance of inflammation for cardiovascular problems (and many other diseases as well). The full paper is here; read the abstract below:

Background Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. Results At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P=0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P=0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P=0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P=0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P=0.31). Conclusions Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846 .).

More Against Red And Processed Meat

By 4028mdk09 - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=25399566

Is enhanced mortality associated more with red meat/processed meat consumption or with saturated fatty acid (SFA) consumption?  Is it the meat or the saturated fats?  A recent study says meat:

Among highly educated persons, aged >45 years, a high consumption of red, total, and red + processed meat was related to increased all-cause mortality, compared with those with low consumption, whereas no significant associations were found for SFA intake. Dietary guidelines should specifically limit meat consumption and not relying only in limiting SFA intake.

And:

…replacing 100 g of vegetables, fruits & nuts or cereals by 100 g of red meat resulted in higher mortality risk.

For older individuals eating more meat, there was some effect of more SFA consumption:

In these participants, SFA intake was non-significantly associated with mortality. However, isocaloric replacement of monounsaturated fat or carbohydrates by SFA resulted in significantly higher mortality risk. 

But overall this particular study provides data pointing the finger at red meat/processed meat.  Given the consistency of this finding with that of previous studies, it looks for now that excessive consumption of red meat/processed meat is a major dietary health risk.  Looking at all studies, SFA risk is more equivocal; this study does not show, overall, a significant risk, but other studies have showed such a risk.

Limiting red meat/processed meat consumption would seem to be a prudent dietary priority.  Limiting SFA may be a good idea as well, depending upon context and whatever other dietary recommendations a person has from their physician, etc., but the meat situation would seem more important at this point.  Who knows what further studies will say about SFA.

Replacing Trans Fats With Something That May Be Just As Bad

Beans, cucumber salad, mushrooms, and eggplant-tomato spread: none of them have IFs, especially if you cook them at home!

The following information is from
Trust the food industry to do the wrong thing:

"Ever since the FDA banned trans fats in June 2015, food manufacturers have been busy training a replacement. 

Just when you think the stuff that bullies your belly was finally kicked out of the game, its just-as-mean teammate gets put in. Conditioned to perform just like its predecessor, Interesterified Fat (IF) appears to be just as lethal. Plus: IF is super-sneaky, essentially flying under the radar and making it easier to be put into your food. It will wreak havoc on your body, just like the trans fats we’ve all been fighting. That’s super frustrating, since there’s a reason it’s one of the 40 Unhealthiest Foods on the Planet! 

IF is a fusion of fats; molecules in naturally-occurring fats are rearranged to create a more shelf-stable model. (Sounds familiar…) These fats include stearic acid, a naturally-occurring saturated fat and vegetable oils, AKA soybean oil, palm oil, palm kernel oil, etc. 

Not much is known about IF—but what is known only confirms that this guy has trained under TF and has adapted his rotten ways. In fact, studies showed that when humans consumed IF, there was an increase in bad cholesterol and a decrease in good. And another study showed that female rodents that ingested this man-made fat had male offspring that were predisposed to diabetes."

Actionable

What should we do?

• The solution to this and similar problems is to end food industry lobbying, break the power of the food industry, and at the same time, educate the consumer. 

• If additives such as the IFs (described above) are hidden from the label, the safest approach is to avoid all processed foods (which is easier said, than done). Learning how to cook meals that are safe and healthy for yourself and your family should be a priority.

Omega-3 Fatty Acids And Prevention Of Colorectal Cancer Recurrence

Omega-3 fatty acids in (recurrent) cancer prevention.

Increasing evidence supports the contention that many malignancies, including sporadic colorectal cancer, are driven by the self-renewing, chemotherapy-resistant cancer stem/stem-like cells (CSC/CSLC), underscoring the need for improved preventive and therapeutic strategies targeting CSCs/CSLCs. Omega-3 polyunsaturated fatty acids (ω-3 PUFA), have been reported to inhibit the growth of primary tumors, but their potential as a preventive agent for recurring cancers is unexplored. The primary objectives of this investigation are (i) to examine whether eicosapentaenoic acid (EPA; one of the ω-3 PUFA) synergizes with FuOx (5-FU+Oxaliplatin), the backbone of colon cancer chemotherapy, and (ii) whether EPA by itself or in combination with conventional chemotherapy prevents the recurrence of colon cancer via eliminating/suppressing CSCs/CSLCs. FuOx-resistant (chemoresistant; CR) colon cancer cells, highly enriched in CSCs, were used for this study. Although EPA alone was effective, combination of EPA and FuOx was more potent in (i) inhibiting cell growth, colonosphere formation, and sphere-forming frequency, (ii) increasing sphere disintegration, (iii) suppressing the growth of SCID mice xenografts of CR colon cancer cells, and (iv) decreasing proinflammatory metabolites in mice. In addition, EPA + FuOx caused a reduction in CSC/CSLC population. The growth reduction by this regimen is the result of increased apoptosis as evidenced by PARP cleavage. Furthermore, increased pPTEN, decreased pAkt, normalization of β-catenin expression, localization, and transcriptional activity by EPA suggests a role for the PTEN-Akt axis and Wnt signaling in regulating this process. Our data suggest that EPA by itself or in combination with FuOx could be an effective preventive strategy for recurring colorectal cancer.

These findings suggest even more health benefits for omega-3 fatty acids.  It would seem that reasonable consumption of certain polyunsaturated fats has not only cardiovascular benefits, but cancer prevention benefits as well.