Buying stuff with cash is explicitly illegal now?

Notes:

Over the past century, consumption in the United States of omega-6 (n-6) fatty acids has increased dramatically, mostly from corn and soybean oil, whereas omega-3 fatty acid intake has remained stable (9). This high omega-6 intake relative to omega-3 fatty acids may contribute to breast cancer risk, because a low omega-3:6 ratio in tissue can create a proinflammatory milieu (5, 6) and thereby promote tumor formation and progression

Assessing this relationship is complicated by problems assessing omega-3 and omega-6 intake from food frequency questionnaires (FFQ; 16) and inconsistent results among different populations

two general conclusions and a hypothesis. First, women consuming their usual diet have a low intake of omega-3 relative to omega-6 fatty acids that is reflected in the omega-3:6 ratio in multiple tissues.

we found inverse associations between tissue levels of long-chain omega-3 fatty acids and omega-3:6 ratios and a reversible biomarker of breast cancer risk

Thoughts:

It would be reasonable to reduce or eliminate dietary omega-6 sources, such as seed oils (vegetable oils) for people who are concerned with breast cancer.

The papers make takeaway about omega-3 supplements is one approach, but I think its being indirect - either the authors believe seed oils are necessary, or they don’t want to get into a fight about removing seed oils from the diet. The advice seems backwards.

I’ll post my notes here.

Some of the salt regulating pathways, have only been considered in terms of water regulation, but these also have a impact on metabolic processes especially in fat cells

Why does sodium matter? It’s essential, without enough sodium the body stops functioning. Electrolyte balance and fluid regulation. Where salt goes, water follows. We need sodium, and other electrolytes, for nerve function. Acid / Base balance - maintaining PH balance. Absorption of nutrients (they follow the sodium from the digestive tract).

Renin Angiotensin Aldosterone System - RAAS - ras. Main system for regulating salt in the body, primary signal is low blood pressure triggering RAAS. Secondary trigger when sodium levels drop. Once its turned on, kidneys release Renin. At the same time the liver produces Angiotensinogen - A hormone/protein. inogen implies it is not in its primary form yet. Renin+Angiotensinogen = Angiotensin1. ACE - Angiotension converting enzyme (produced by the lungs - which actually are a endocrine gland!) + Angiotension1 = Angiotensin 2.

Angiotensin 2 - elicits powerful vasoconstriction - restoring blood pressure by narrowing blood vessels. Also has a anti-diuretic effect. Stimulates thirst centers - drinking water will help restore blood volume and pressure. Most famously - in the Adrenal cortex and stimulates the production of aldosterone.

Aldosterone has a powerful effect in the kidneys to reabsorb any sodium that had been removed from the blood, and reintroduced into the blood. The theory being the body is setting up the stage to encourage osmosis for water to correct blood pressure.

This system has a built in negative feedback loop, once aldosterone has stimulated the kidney effect, the RAAS system should shutdown as the stimulants are removed.

Anti-hypertension medications interfere with this system. ACE inhibitors - block the ACE from the lungs in the above cycle. Also Angiotension Receptor blockers.

Insulin also has an effect on salt handling. Part of its anabolic effects - you need more electrolytes to grow. Insulin directly stimulates sodium reabsorption in the kidney tubules particularly in the distal part. This activity is mediated by insulins effect on sodium potassium pumps - driving more sodium back into the body. Insulin also has a heavy impact on the RAAS system via sympathetic nervous system increasing renin production and thus the RAAS cycle resulting in higher aldosterone (which even more aggressively collects sodium). Insulin also enhances vascular sensitivity to Angiotensin 2 - increasing the vasoconstriction effect (restoring/increasing blood pressure).

People who are deficient in salt (such as a low salt diet), chronically triggering the RAAS system - and insulin levels - in a attempt to compensate for the low sodium levels. Therefor mechanistically salt restriction increases insulin resistance (there is a study -Lastra 2010, Sharma 1999 Maybe?.

Fat cells - have receptors for both Aldosterone, Angiotensin 2

Aldosterone receptors - mineralocorticoid receptors. Corticoid means it coming from the cortex of the adrenal gland, mineralo evokes minerals i.e. salt. When aldosterone binds to fat cells, stimulates fat cell growth (hypertrophy).

Angiotensin 2 - Many receptors - stimulates the expression of multiple lipogenic (synthesis of fat) enzymes, turns on fatty acid synthes, and acetyl coa carboxylase (links carbons) - the combination will take carbons and create new fat cells. Can also promote fibrosis of fat cells, key development for fat cell going from insulin sensitive to insulin resistant state (promoting inflammation). Therefor Angiotension 2 promotes inflammation in the fat cells. ppar gamma is activated as well, and tells proto-cells to become fat cells.

When insulin binds to its receptor on a cell, a signaling cascade, but with Angiotensin 2 is involved it disrupts/antagonizes this signal chain.

No signal in the body can promote fat cell growth in the absence of insulin.

TLDR - Salt is good

However, the absence of association between low carbohydrate intake (eg, <50% of energy) and health outcomes does not provide support for very low carbohydrate diets. Importantly, a certain amount of carbohydrate is necessary to meet short-term energy demands during physical activity and so moderate intakes (eg, 50–55% of energy) are likely to be more appropriate than either very high or very low carbohydrate intakes

This conclusion seems to be outside of the data collected. They are making the link between very low carbohydrate diets (<50%, so 49%), and “short term energy demands”. This is linking a preconceived notion to a misnomer term. In the low carb high fat research sphere, 49% would be considered high carb, and well outside of the level needed to maintain nutritional ketosis. It doesn’t even touch upon gluconeogenesis and the fact it is established in nutritional literature there isn’t a thing such as a essential carbohydrate. Note the lack of references for this statement

This also makes the assumption that there we would see a linear benefit for carbohydrate reduction, its a theory that should be tested, not assumed. (It’s a step function, with nutritional ketosis/insulin sensitivity being the step)

This is a great paper, doing good research, but I think its overstepping its remit making conclusions / recommendations for properties it was not studying.