Hydration: Attempt Only Under Medical Supervision

I've noticed how the word "hydration" has crept into the popular lexicon in the last decade or so. Before that, we were so primitive, we just "drank water". Now you need a PhD just to put a glass to your lips. I'm not sure I'm qualified!

I've been hearing so many people, including health professionals, tell me to drink 8 glasses of water a day for my entire life. In my middle school health class, I was told by my hydrophilic teacher that I should be urinating every hour and my urine should always be clear. For my whole life, I've thought it was nonsense. Yet the message has reached people. Walk around any college campus and you'll see undergrads faithfully carrying around their endocrine-disrupting plastic-water everywhere they go.

You see, our bodies have this very sophisticated mechanism to ensure water homeostasis. It's called thirst. If we need so much water to be healthy, why aren't we thirsty more often?

I skimmed through a paper today in the Journal of the American Society of Nephrology that reviews the evidence for health benefits from drinking more water than your thirst demands. Their conclusion: there's no evidence to suggest it helps anything. Water is just a nice harmless placebo.

The term "hydration" has helped fuel a whole industry to satisfy our need for hydration technology. Gatorade claims it hydrates better than water. It must be the high-fructose corn syrup and yellow #5... And make sure to bring your "hydration pack" when you go on your 20 minute jog; you might get lost and end up in the Kalahari desert!

I actually think the water craze isn't totally harmless. Drinking large amounts of water with a meal interferes with digestion by diluting digestive enzymes and stomach acid. Drinking a tall beer does the same. Wine is better because it tends to be a smaller volume.

As far as I'm concerned, with minor exceptions, the only thing to drink is water. I'll have an occasional glass of wine, beer or whole raw milk, but 99% of what I drink is good old-fashioned dihydrogen oxide.

The only time I drink a large amount of water without being thirsty is if I'm about to do vigorous exercise or spend time outside in hot weather.

Thanks to Snap for the CC photo.

Low-carb Review Article

The other day, I came across this nice review article from the American Journal of Clinical Nutrition. It gives a thorough but accessible overview of the current state of research into carbohydrate-restricted diets, without all the fatophobic mumbo-jumbo. It points out a few "elephants in the room" that the mainstream likes to ignore. First of all, the current approach isn't working:

The persistence of an epidemic of obesity and type 2 diabetes suggests that new nutritional strategies are needed if the epidemic is to be overcome.

They claim that preagricultural diets were low in carbohydrate:

In contrast to current Western diets, the traditional diets of many preagricultural peoples were relatively low in carbohydrate (1, 2). In North America, for example, the traditional diet of many First Nations peoples of Canada before European migration comprised fish, meat, wild plants, and berries. The change in lifestyle of several North American aboriginal populations occurred as recently as the late 1800s, and the numerous ensuing health problems were extensively documented (3-5). Whereas many aspects of lifestyle were altered with modernization, these researchers suspected that the health problems came from the change in nutrition—specifically, the introduction of sugar and flour.

But of course, many of them were very high in carbohydrate, and these cultures seemed in fine health as well.

Carbohydrate reduction leads to a normalization of appetite:

It may also be that the mere lowering of serum insulin concentrations, as is seen with LCDs, may lead to a reduction in appetite. In support of this idea, several studies have found that insulin increases food intake, that foods with high insulin responses are less satiating, and that suppression of insulin with octreotide leads to weight loss (27-29).

I can't believe it; all that fat isn't going to clog my arteries??

Several outpatient diet studies have shown reductions in CVD risk factors after an 8–12-wk LCKD, during weight loss, and during weight maintenance (21, 60-62).

The last paragraph is a zinger:

We emphasize that strategies based on carbohydrate restriction have continued to fulfill their promise in relation to weight loss and that, contrary to early concerns, they have a generally beneficial effect on most markers of CVD, even in the absence of weight loss. In combination with the intuitive and established efficacy in relation to glycemic control in diabetics, some form of LCD may be the preferred choice for weight reduction as well as for general health.

Cegah Stroke, --- Konsumsi Wortel

KapanLagi.com - Stroke bukan monopoli penyakit orang tua, orang yang masih muda pun banyak yang terserang penyakit ini. Walaupun penyakit ini sering didominasi orang tua, tetapi fakta menunjukkan, banyak orang mati muda karena terserang stroke. Boleh dibilang, penyakit stroke menyerang kepada siapa saja tanpa memandang usia.

STROKE

Stroke adalah gangguan fungsi otak akibat aliran darah ke otak mengalami gangguan. Akibatnya nutrisi dan oksigen yang dibutuhkan otak tidak terpenuhi dengan baik. Penyebab stroke bisa karena adanya sumbatan di pembuluh darah dan adanya pembuluh darah yang pecah. Stroke yang diderita oleh orang tua karena proses penuaan yang menyebabkan pembuluh darah mengeras dan menyempit, dan adanya lemak yang menyumbat pembuluh darah.

Sementara penyebab Stroke pada usia remaja dan usia produkti (15 samoai 40 tahun) disebabkan karena stres, penyalahgunaan narkoba, alkohol, faktor keturunan dan gaya hidup yang tak sehat.

Stroke merupakan salah satu penyebab kematian terbanyak, penyakit ini sering diidentikkan dengan kelumpuhan anggota gerak yang menyerang secara tiba-tiba serta terjadinya penurunan kesadaran. Justru gejala tersamar dari stroke kurang diwaspadai, seperti gangguan memori, gangguan emosi, gangguan perilaku. Padahal deteksi dini terhadap gejala stroke merupakan hal yang utama.

Banyak cara dilakukan orang untuk menghindari penyakit ini, salah satu cara yang paling mudah dan murah adalah mengkonsumsi tanaman wortel.

WORTEL

Wortel dikenal memiliki kandungan Vitamin A yang sangat tinggi, selain memiliki unsur lain seperti kalori, protein, lemak, hidrat arang, kalsium, dan besi. Wortel termasuk tumbuhan yang ditanam sepanjang tahun, terutama di daerah pegunungan yang memiliki suhu udara dingin dan lembab, dan tumbuhan ini dapat tumbuh pada semua musim.

MANFAAT WORTEL PADA PENYAKIT STROKE
Selama ini orang mengenal wortel hanya untuk kesehatan mata karena kandungan vitamin A yang sangat tinggi. Ternyata tanaman ini mempunyai khasiat yang lebih hebat lagi. Sayuran yang dikenal sebagai makanan favorit kelinci ini ternyata bisa mencegah stroke. Orang yang terkena stroke, jika banyak mengkonsumsi Vitamin A, akan mengalami lebih sedikit kerusakan neurologis (saraf) dan mempunyai kesempatan untuk sembuh. Hal ini disebabkan karena waktu otak tidak memperoleh oksigen berapa lama, seperti pada stroke, sel mulai mengalami malfungsi (gangguan fungsi) yang menyebabkan rangkaian kejadian mencapai puncaknya ketika pada sel-sel saraf terjadi kerusakan oksidatif, dan kondisi tersebut dapat diredam jika dalam darah banyak terdapat vitamin A.

Sebuah penelitan menunjukkan, mengkonsumsi wortel sedikitnya lima kali dalam seminggu dapat menurunkan resiko terkena stroke hingga 68 persen bila dibandingkan yang makan wortel satu kali dalam sebulan.
Khasiat antistroke tersebut juga ditimbulkan karena aktivitas beta karoten yang mencegah terjadinya plak atau timbunan kolesterol dalam pembuluh darah. Beta karoten merupakan pigmen paling aktif apabila dibandingkan dengan alpha dan gamma karoten. Biasanya beta karoten lebih dikenal sebagai provitamin A yang akan menjadi vitamin A pada dinding usus halus.
Tak ada seorangpun yang mau terkena stroke, dan tak seorangpun yang ingin mati muda. Mencegah lebih baik daripada mengobati, belajar pada alam, karena dari alam kita banyak menemukan manfaat. Wortel yang kita kenal sebagai sayuran, ternyata bisa menjauhkan kita dari kematian. (sud)

Visceral Fat and Dementia

This study was released today, demonstrating in 6,583 patients that visceral fat mass in the 40s predicts the risk of dementia in old age. Patients in the highest quintile (20% with the most visceral fat mass) had an almost three-fold higher risk of dementia than patients in the lowest quintile. Overall fat mass was less strongly correlated with dementia. This study is so timely, they must have heard about my blog post.

They used a measure of visceral fat called the "sagittal abdominal diameter", basically the distance from the back to the belly button. In other words, the beer belly.

What we're looking at is another facet of the pervasive "disease of civilization" that rolls into town on the same truck as sugar and white flour. Weston Price described it in 14 different cultures throughout the world in Nutrition and Physical Degeneration. Diabetes, cardiovascular disease, obesity, cancer and dementia all seem to come hand-in-hand. It's hard to say exactly what the root cause is, but the chain of causality seems to pass through visceral fat in many people.

Visceral Fat

This week, I stumbled upon a very interesting series of articles from the lab of Dr. Nir Barzilai.

The first article I came across showed that surgical removal of the visceral fat deposit of rats increased their lifespan. Visceral fat (VF) is the "beer belly", and consists of the perinephratic fat around the kidneys and the omental fat in front of the intestines. It doesn't include subcutaneous fat, the fat layer under the skin.

VF is tightly associated with the metabolic syndrome, the quintessential "disease of civilization" that affects 24% of Americans (NHANES III). It's defined by three or more of the following criteria: high blood pressure, large waist circumference, low HDL cholesterol, high triglycerides, and high fasting glucose. The metabolic syndrome is associated with a 3-4-fold increase in the risk of death from cardiovascular disease, and a 6-fold increase in the risk of developing type II diabetes. From a review on the metabolic syndrome (parentheses mine):

The most common alteration related to the impaired glucose metabolism with aging is the progressively increased fasting and postprandial [post-meal] plasma insulin levels, suggesting an insulin-resistant state.

This is all well and good, but who cares? What's to say VF plays any role other than as a simple marker for overweight?

The longevity paper led me to Dr. Barzilai's previous papers, which answered this question rather thoroughly. Rats raised on standard rat chow, which is a sad little compressed pellet made of grains and added nutrients, develop elevated insulin and insulin resistance with age, just like humans. Unless they don't have VF. Rats that had their VF surgically removed did not develop insulin resistance or elevated insulin with age, despite rebounding to their original total fat mass rather quickly (VF accounts for ~18% of total fat in these rats). These parameters are unaffected by removing an equal amount of subcutaneous fat, which has been shown in human liposuction patients as well.

Removing VF also improved diabetes-prone Zucker rats, which are profoundly insulin-resistant (leptin receptor loss-of-function). It kept wild-type rats just as insulin-sensitive as calorically restricted controls, which had a small amount of VF. This shows that VF isn't just a passive player; it's essential for the development of insulin resistance. It also shows, along with human studies, that insulin resistance is not an inevitable consequence of aging.

Adipose (fat) tissue is being increasingly recognized as an important endocrine (hormone-secreting) organ. It produces many different hormones that affect insulin sensitivity and appetite regulation, among other things. These hormones are collectively known as fat-derived peptides (FDPs). At least one of these FDPs, TNF-alpha, promotes insulin resistance.

Dr. Barzilai's group went on to explore the mechanism of VF contributing to insulin resistance. They increased the rate of glucose flux into the fat tissue of rats by infusing either glucose or insulin into the bloodstream. These treatments both cause increased glucose uptake by fat cells. What they saw when they dissected the rats was striking. The VF had ramped up its production of FDPs from 2- to 15-fold, while the subcutaneous fat had barely changed. Incidentally, insulin increased glucose uptake by VF twice as much as subcutaneous fat.

I'll say this again, because it's important. They forced glucose into VF cells, and those cells dramatically upregulated FDP production. And again, no visceral fat, no FDPs.

In earlier papers, he also showed that the removal of VF dramatically reduces the expression of TNF-alpha and leptin (two FDPs) in subcutaneous fat on a longer timescale, showing that VF and subcutaneous fat communicate to alter the metabolism. Again, TNF-alpha promotes insulin resistance, making it a possible link between the fat tissue and peripheral effects. VF removal had no effect on triglycerides, suggesting that they're only a marker of insulin dysfunction rather than a cause.

Now to take this research to its logical conclusion. Here's a plausible sequence of events leading up to the metabolic syndrome:

• A meal high in quickly digested carbohydrate elevates blood glucose. OR, excessive fructose causes insulin resistance in the liver which leads to high fasting glucose.
  

• Visceral fat responds by increasing production of FDPs.

• FDPs, directly and/or indirectly, cause insulin resistance in the liver, muscle and other tissue. Liver insulin resistance causes alterations in lipoprotein ("cholesterol") profile (more on this in another post). Fat tissue remains insulin-sensitive.

• The vicious cycle continues, with increased visceral fat size and glucose uptake increasing FDP production, which makes the liver more insulin resistant, which increases glucose production by the liver, etc.