Brown Fat and the Cat in the Hat

My son Paul made this

My son Paul made this (I’ll see you in heaven, Romeo)

The Joslin diabetes blog has an interesting article on brown fat and its effect on metabolic rate and insulin sensitivity. Brown fat is just a type of body type different from the more plentiful white fat (which is actually more pale yellow). If there are other colors of body fat, I don’t know.

If you can “activate” your brown fat, it helps you burn more calories, which could be helpful if you’re trying to lose weight. It also improves insulin sensitivity: beneficial if you have type 2 diabetes or are prone to it.

From Joslin:

“When brown fat is fully activated, it can burn between 200 and 300 extra calories per day. It is most successfully activated through cold exposure. A recent study of people with type 2 diabetes had volunteers sit in a 50 degree room for a couple of hours a day for 10 days in shorts and short-sleeved shirts.

“When I say cold, it’s not icy cold, it’s not like the winter in Boston,” she says. “It’s more or less like the temperature we have here in autumn. After this mild cold exposure, all ten volunteers with type 2 diabetes, as shown in that study, displayed increased brown fat activity and improved insulin sensitivity. This is very exciting.”

Dr. Tseng is working on understanding exactly what is happening on a cellular level to activate brown fat in the cold to see if she can create a drug that will mimic the effects. “Although cold works, it’s just not pleasant,” she says. “If you had to sit in a cold room for a few hours every day, perhaps not everybody could accept that.”

Source: How Your Body Temperature Can Affect Your Metabolism | Speaking of Diabetes | The Joslin Blog

Another way to activate brown fat is exercise (at least if you’re a man or a mouse).

Steve Parker, M.D.

We Don’t Know How to Get Overweight Kids to Exercise

From a recent meta-analysis:

“In conclusion, there is no evidence that currently available interventions are able to increase physical activity among overweight or obese children. This questions the contribution of physical activity to the treatment of overweight and obesity in children in the studied interventions and calls for other treatment strategies.”

Source: Effectiveness of interventions on physical activity in overweight or obese children: a systematic review and meta-analysis including studies with o… – PubMed – NCBI

For weight loss in overweight and obese children, you have to focus on diet modification. Same as adults.

My Fellow Americans: How About Paying 80% Less for Your Healthcare?

Karl Denninger has a plan that he thinks would reduce the cost of healthcare in the U.S. by up to 85%!

Almost one in every five dollars spent in the U.S. is for “healthcare.” That’s probably the highest percentage of any country, and I don’t think we’re getting our money’s worth.

Karl’s plan hinges on the reality that the healthcare system here is not operating as a free market. There’s too much price-fixing, lack of price transparency, lack of competition, and consumer fraud done by collusion among the big players, such as health insurers, hospitals, physicians, and politicians. Karl says such practices have been illegal for decades, but applicable laws simply have not been enforced by the powers that be.

I’ve always had the impression that health insurers were exempt from anti-trust laws. Karl says that ain’t so.

Read the whole thang if you’re interested in U.S. healthcare reform. For example:

I’ve repeatedly, over some 30 years time, heard that there’s “some law” that exempts health care from anti-trust [laws] when the discussion turns to the topic of price-fixing, collusion, differential billing for commodities of like kind and quantity and similar. Every time I hear this claim I respond the same way: “Show me the law.”

Nobody ever has.

And I haven’t asked just once or twice. I’ve asked dozens of times since the 1990s. I’ve asked politicians. I’ve asked lawyers. I’ve asked political candidates. I’ve asked policy “wonks” of various flavors. Gary Johnson got asked (Lib candidate for President) in person a number of years back in his suite during the Libertarian convention in Orlando. Yet not one of the people I’ve asked has ever replied with a title, chapter and section of US code that provides such an exemption.

As just one of many examples I heard this claim during the campaign from a (Democrat) candidate for the US House when I asked him whether he would demand that the executive enforce anti-trust law against all medical providers and suppliers. He said he’d call me with a cite to the law when I responded that with all due respect the exemption he claimed did not exist at a meet-and-greet in a room full of Libertarians. He never did call me. (He lost the election, incidentally.)

I’m utterly convinced that’s because the oft-claimed exemption doesn’t exist. I’m in fact quite sure of it, because I can actually read the US Code — it’s public, of course, and the sections that could bear on this matter are reasonable in size (that is, I can and have read through them in a day or two.)

Never mind the contravening evidence too – like this case from 1979 that went to the Supreme Court which ruled that Mccarran-Ferguson does not protect insurance companies against anti-trust claims related to drug “discounts” on collusive actions. In other words the insurance company took the case to the Supreme Court and lost, which is damn good evidence that (1) anti-trust does apply to health care broadly including the criminal provisions in the Sherman and Clayton Acts and (2) health insurance firms and providers are not exempt to the extent they collude to restrain trade or fix prices.

It is thus my considered position that the reason the law isn’t enforced isn’t because it doesn’t apply — it isn’t enforced because the Executive voluntarily chooses to refuse to enforce it in collusion with Congress and the States and has done so for 30+ years despite the evidence being clear that the law — a law that carries both ruinous civil and felony criminal penalties — is being violated on a daily, continuing basis by the entirety of the so-called “health system.”

Sheila Kealey on Turmeric: Healthy or Hype? 

“Although many studies have investigated turmeric/curcumin, and some have shown promise, at this point these findings aren’t good enough evidence to suggest that consuming turmeric improves any health condition.  It’s important to consider the preliminary nature of the research and recent review questioning of curcumin’s biological activity. Turmeric is certainly not a cure-all panacea as some have touted.  More research may help uncover specific benefits to curcumin or other compounds in turmeric.”

Source: Healthy or Hype? Turmeric – Sheila Kealey

Found: Another Green Tea That’s Actually Green

Yes!

Yes!

My wife found this “matcha LOVE™” Japanese green tea at Sprouts market. A worker said it’s a favorite of their Japanese ethnic patrons.

I don’t know what she paid for it; at Amazon.com you can get 10 teabags for $12 something (USD). So it’s expensive. Some of the other teas I’ve reviewed here are 18 cents a cup.

The flavor is fine, a bit stronger than many “green” teas I’ve tried. That’s not bad. A nice esthetic bonus is that the brewed tea stayed green to the last drop. Several other green teas I’ve tried turn tan after a few minutes.

Steve Parker, M.D.

How a single high-fat “meal” (palm oil) affects liver metabolism 

I thought we were through demonizing saturated fats.

I put my headline’s “meal” in quotes because the only item in the meal was palm oil. That doesn’t look like one of my meals.

From MNT:

“Individuals who consume higher levels of saturated fats are more likely to feel the effects of a range of health conditions, including non-alcoholic fatty liver disease. Although this link is well-known, exactly how and why it develops is not yet clear.

Recent research investigates the effects of a single high-fat meal on the liver.Non-alcoholic fatty liver disease (NAFLD), as the name suggests, is a condition in which excess fat is stored in the liver of an individual who drinks little or no alcohol.

Marked by liver inflammation, NAFLD most commonly affects people in their 40s and 50s, and especially those who are obese. It can cause scarring of the liver and permanent damage. At its worst, it can lead to liver failure.NAFLD is primarily characterized by an increased buildup of fat in the liver, and this buildup is often accompanied by insulin resistance, thereby increasing the risk of type 2 diabetes and cardiovascular disease.”

Source: How a single high-fat meal affects liver metabolism – Medical News Today

German researchers fed a single palm oil meal to 14 healthy men, and some mice.

The article writer doesn’t make it clear whether results apply to the men, the mice, or all combined. Anyway, they found

  • Elevated blood triglycerides
  • Increased glucagon (a pancreas hormone that raises blood sugar)
  • Whole body insulin sensitivity decreased 25 percent
  • Hepatic insulin sensitivity decreased 15 percent
  • Adipose (fat) tissue insulin sensitivity decreased 34 percent
  • Triglycerides in the liver – the main constituent of body fat in humans  – also rose by 35 percent

All of these changes would tend to promote not only NAFLD but also type 2 diabetes.

Whether these adverse changes would be see with other saturated fats or polyunsaturated fats is left unstated in the report.

From UpToDate.com: “The pathogenesis of nonalcoholic fatty liver disease has not been fully elucidated. The most widely supported theory implicates insulin resistance as the key mechanism leading to hepatic steatosis, and perhaps also to steatohepatitis. Others have proposed that a “second hit,” or additional oxidative injury, is required to manifest the necroinflammatory component of steatohepatitis. Hepatic iron, leptin, antioxidant deficiencies, and intestinal bacteria have all been suggested as potential oxidative stressors.”

I’ve been hearing for years that NAFLD is going to be a big deal. At least every other shift I work in the hospital, I see someone with evidence for fatty liver on ultrasound or CT scan.

The mainstay of therapy for NAFLD is weight loss for those who are obese or overweight. It’s probably a good idea to avoid all alcohol consumption, too.

If you need to lose weight, check out my books.

Steve Parker, M.D.

Steve Parker MD, Advanced Mediterranean Diet

Two diet books in one

 

Unified theory of Alzheimer’s disease (UTAD): implications for prevention and curative therapy

No need to read the following. It’ll likely bore you to death. I record it here for my own purposes. Alzheimer’s Disease is a huge problem and we desperately need ways to prevent and cure it. Prevention should be easier than cure. BTW, the Mediterranean diet is linked to lower risk of Alzheimer’s Disease.

“The master regulator/inhibitor of autophagy is the mammalian target of rapamycin (mTOR). This intracellular kinase functions as a key signalling node that integrates information regarding extracellular growth factor stimulation, nutrient availability and energy supplies. The fungal metabolite rapamycin was accidently found to block mTOR and became not only the eponym of mTOR but also the main molecular tool to dissect mTOR-function. Rapamycin treatment was found to activate autophagy by inhibiting mTOR, thereby slowing down both aging and cognitive decline of caged mice, suggesting that inefficient autophagy as part of the NRJ-program might be a central element of both processes. Conversely, caging (standard housing) might eliminate an important behavioural cues (like for instance physical activity or intermittent fasting, see below), which leads to unnaturally high activity of mTOR and low activity of peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), the master controller of mitochondrogenesis (see below), thereby inhibiting neuron-rejuvenating and protecting autophagy. Hence the observed aging and cognitive decline in murine models of AD might be regarded as artificial and not reflecting the aging process under natural conditions.

Other behavioural cues that inactivate mTOR are, besides physical exercise, which was shown to promote autophagy of defunct organelles and macromolecules in the brain, chronic caloric restriction (CCR), which is well known to delay aging and extend life-span in essentially all eukaryotic organism. But is CCR a physiological cue or rather an artefact of experimental research that simulates, to some extent, a more natural dietary pattern, namely intermittent fasting (IMF), which from an evolutionary point of view is more natural (see below)? But IMF is experimentally more labour-intensive than CCR and therefore less well studied. Nevertheless, autophagy and in particular mitophagy was found to being activated by CCR through inhibition of mTOR in essentially all species investigated, ranging from yeast, to flies, worms, fish, rodents and even to rhesus monkeys [87], thereby decelerating mTOR-driven aging. CCR not only extends lifespan, it also protects the central nervous system from neurodegenerative disorders, whereas excessive caloric intake is clearly associated with accelerated aging of the brain and increased the risk of neurodegenerative disorders due to suppressed autophagy.

Nevertheless, IMF was shown to create a more robust and steady inhibition of mTOR-accelerated aging and cognitive decline when compared to CCR. This is explained by the fact that the main hormone-like signalling molecules of the metabolic status during IMF, the ketone bodies acetoacetate (AcAc) and D-β-hydroxybutyrate (βOHB), are more efficiently generated during fasting than by CCR. These two respiratory fuels can endogenously be produced by the liver in large quantities (up to 150 g/day) from mobilized fatty acids in a variety of physiological or pathological conditions. In humans, basal serum levels of βOHB are in the low micromolar range, but rise up to several hundred micromole after 12 to 16 h of fasting. Importantly, when blood glucose and insulin are low, up to 60 % of the brain energy needs can be derived from ketone bodies, replacing glucose as its primary fuel. Similar high levels of up to 1 to 2 millimole βOHB are reached after prolonged endurance exercise. A physiologically relevant increase in ketone body production is already achieved by fasting overnight, which can even be enhanced if we are physically active before breaking the fasting in the morning. This most likely mimics the situation that faced our foraging ancestors who went out for hunting or gathering food with their stomachs empty.

Since neither long- nor medium-chain saturated fatty acids can pass the BBB, only their transformation into ketone bodies allows our energy-demanding brain to access the largest energy store, our adipose tissue. In fact, ketone body production reduces glucose requirement and preserves gluconeogenic protein stores during fasting, which enables a profound increase in the capacity for survival. Interestingly and again in line with the GMH, elderly generate ketone bodies at least as efficient as younger adults during IMF and the metabolic response to a ketogenic diet appears also to be unaffected by aging.As hinted at above, the observation that IMF is superior to CCR makes also a lot of sense from an evolutionary perspective, as not chronic starvation but rather periodic alteration between fasting and intake of high-caloric meals after successful foraging was ancient normality. Importantly, recent evidence suggests that our phylogenetically conserved genetic program uses the metabolic changes that originate from intermittent fasting (IMF) as a behavioural cue of for [sic] the initiation of subcellular renewal. This is a good thing, since in order to maintain cellular youth, we do not have to starve by CCR. It is sufficient to alternate phases of fasting, which just need to be sufficiently long to induce ketone body production (for instance 12 h overnight) and phases of eating, in which the total energy demand of our body can be met. In contrast, current normality consists of constant feeding pattern, which results in permanent high mTOR activity (and low PGC-1α-levels, see below), which suppresses cellular rejuvenation. A sedentary lifestyle aggravates this pro-aging effect, whereas prolonged physical exercise reduces mTOR-activity, possibly also by increasing ketone body production.”

Source: Unified theory of Alzheimer’s disease (UTAD): implications for prevention and curative therapy