PURE Study: Higher Carb Consumption Linked to More Deaths

Here’s the abstract of a new epidemiological study that investigated the relationships between diet, cardiovascular disease, and death rates. I don’t have the entire article. My sense is that the 18 countries studied are mostly non-Western:


The relationship between macronutrients and cardiovascular disease and mortality is controversial. Most available data are from European and North American populations where nutrition excess is more likely, so their applicability to other populations is unclear.


The Prospective Urban Rural Epidemiology (PURE) study is a large, epidemiological cohort study of individuals aged 35–70 years (enrolled between Jan 1, 2003, and March 31, 2013) in 18 countries with a median follow-up of 7·4 years (IQR 5·3–9·3). Dietary intake of 135 335 individuals was recorded using validated food frequency questionnaires. The primary outcomes were total mortality and major cardiovascular events (fatal cardiovascular disease, non-fatal myocardial infarction, stroke, and heart failure). Secondary outcomes were all myocardial infarctions, stroke, cardiovascular disease mortality, and non-cardiovascular disease mortality. Participants were categorised into quintiles of nutrient intake (carbohydrate, fats, and protein) based on percentage of energy provided by nutrients. We assessed the associations between consumption of carbohydrate, total fat, and each type of fat with cardiovascular disease and total mortality. We calculated hazard ratios (HRs) using a multivariable Cox frailty model with random intercepts to account for centre clustering.


During follow-up, we documented 5796 deaths and 4784 major cardiovascular disease events. Higher carbohydrate intake was associated with an increased risk of total mortality (highest [quintile 5] vs lowest quintile [quintile 1] category, HR 1·28 [95% CI 1·12–1·46], ptrend=0·0001) but not with the risk of cardiovascular disease or cardiovascular disease mortality. Intake of total fat and each type of fat was associated with lower risk of total mortality (quintile 5 vs quintile 1, total fat: HR 0·77 [95% CI 0·67–0·87], ptrend<0·0001; saturated fat, HR 0·86 [0·76–0·99], ptrend=0·0088; monounsaturated fat: HR 0·81 [0·71–0·92], ptrend<0·0001; and polyunsaturated fat: HR 0·80 [0·71–0·89], ptrend<0·0001). Higher saturated fat intake was associated with lower risk of stroke (quintile 5 vs quintile 1, HR 0·79 [95% CI 0·64–0·98], ptrend=0·0498). Total fat and saturated and unsaturated fats were not significantly associated with risk of myocardial infarction or cardiovascular disease mortality.


High carbohydrate intake was associated with higher risk of total mortality, whereas total fat and individual types of fat were related to lower total mortality. Total fat and types of fat were not associated with cardiovascular disease, myocardial infarction, or cardiovascular disease mortality, whereas saturated fat had an inverse association with stroke. Global dietary guidelines should be reconsidered in light of these findings.

Source: Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study – The Lancet

Dementia Rates Are Falling In The U.S.

“An important new national study finds that, after adjusting for age, Americans 65 and older are less likely to get dementia than in the past. The report, published in the Journal of the American Medical Assn (JAMA) confirms previous regional studies in the US as well as recent research in Europe. The reasons for this decline in prevalence of the many dementia-related diseases are complicated, but may be related to higher educational levels. Whatever the cause, the news is positive.”

Source: Dementia Rates Are Falling In The U.S.

Lithium as a Preventative or Treatment of Alzheimer’s Disease

The following excerpt is boring, so move along now. It’s from a recent review article on all the potential causes and therapeutic options for Alzheimer’s Disease (AD). I post it here so I can find it later. Click the link at bottom to RTWT.

“Lithium is not yet generally recognized as a trace element but several lines of evidence make it a strong candidate. For instance, long-term low-dose exposure to lithium exerts anti-aging capabilities and unambiguously decreases mortality in animal models. In humans, epidemiological studies indicate an inverse correlation between lithium concentration in drinking water and mood, depression and suicide rates, amongst other psychiatric conditions. In a study that compared elderly bipolar patients (who exhibit a higher risk for dementia) who had received chronic lithium treatment, with bipolar patients who had not received lithium, it was shown that the prevalence of the treated group was equivalent to the general, age-comparable population, whereas the non-lithium-treated patients had an incidence of dementia that was six times greater, i.e. 5 % vs. 33 %, respectively. In another study it was shown that lithium treatment resulted in an increase in volumes of the hippocampi in both hemispheres compared to an unmedicated group, an effect that was apparent even after a brief treatment period of about 4 weeks on average. Importantly, intake of lithium not only in standard therapeutic but also in trace doses reduces the risk for dementia, suicide, and other behavioural outcomes, suggesting an pharmacological interference with key regulators of these pathological processes. So, lithium naturally regulates critical cell signalling pathways and a lack of lithium in the diet can therefore cause increased disease risk.It has been shown that lithium modulates negatively the activity of the two kinases GSK-3α and GSK-3β, which might explain both the relative specificity and sensitivity of the effects of low-dose lithium treatment (see below). Since GSK-3β-activation by oligomeric Aβ promotes neuroinflammation, phosphorylation of tau and disturbance of AHN [adult hippocampal neurogenesis], all key mechanisms in the AD process, in inhibition of GSK-3 by lithium results in reduced tauopathy and neurodegeneration in vivo. Likewise, lithium treatment was shown to improve AHN, neuropathology and cognitive functions in a mouse model of AD. Furthermore, such “AD-mice” treated from two months of age had decreased numbers of senile plaques, no neuronal loss in cortex and hippocampus and increased BDNF levels when compared to non-treated transgenic mice. In order to achieve this effect, it was sufficient to give lithium at about one per mill of the high standard-dose therapy in bipolar disorder, a dose which can cause some significant side effects. Hence the authors of the study believe that their data support the use of (virtually side-effect free) microdose lithium in the prevention and treatment of Alzheimer’s disease.Indeed, long-term lithium treatment already provided preliminary evidence of its disease-modifying properties for amnestic MCI [mild cognitive impairment] in a randomised controlled trial, where the lithium-treated group had fewer conversions from MCI to AD. Lithium treatment was associated with a significant decrease in cerebrospinal fluid concentrations of hyperphosphorylated tau and better performance on the cognitive subscale of the Alzheimer’s Disease Assessment Scale and in attention tasks. At a more advanced stage of AD, microdose treatment with only 300 μg lithium administered once daily stabilized the AD patients during the complete evaluation phase of 15 months. For instance, whereas the treated group showed no decreased performance in the mini-mental state examination (MMSE), lower scores were observed for the control group during the same period, with significant differences occurring after three months, and increasing progressively.Importantly, lithium, besides being required for efficient AHN and blocking AD-specific pathological processes, also impacts on cell-rejuvenating autophagy. Lithium was found to inhibit the activity of inositol monophosphatase (IMPase), which leads to a decrease of myo-1, 4, 5-triphosphate (IP3). This reduction of IP3-activity induces autophagy, independent of mTOR. In this context it is important to note that lithium chloride extends the lifespan of the nematode Caenorhabditis elegans, possibly by means of mitochondrial rejuvenation, which suggests that lithium exerts its effects on evolutionary highly conserved mechanisms. Intake of drinking water with comparable low lithium concentrations were found to be inversely correlated with all-cause mortality in a large epidemiological study in Japan. Hence a lack of lithium is linking aging and frailty (all increasing mortality) to disturbed autophagy, and AD to impaired AHN, and, thus, might represent another important and modifiable risk factor in this neurodegenerative disease. Traces of lithium can be ingested in some geographic areas by drinking local tap water or otherwise by consuming commercially available, mineral-rich spring waters, containing suitable concentrations of around 1 mg lithium per litre. Hence microdose lithium intake by means of one or two glasses of such water a day is not only of potential therapeutic value (see below) but also a safe preventive measure, by means of simply reducing an intake-deficit of an important novel trace element.”

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

Bonus excerpt:

“Taken together, besides the importance of IMF and physical exercise, also dietary MCTGs [medium-chain trigylcerides] can be an attractive (indirect) source of ketone bodies during the non-fasting state. The intake of coconut oil as a healthy source of MCTGs has additional positive effects on neuronal insulin resistance, neuroinflammation as well as Aβ-toxicity, improves the LDL/HDL-cholesterol quotient by increasing HDL, and ameliorates several others key progression factors of AD. Hence the use of virgin coconut oil is highly recommended as a safe and healthy alternative for polyunsaturated oils for frying and baking and butter and an important part of a comprehensive strategy for the prevention and treatment of AD.”

QOTD: Abraham Lincoln, White Supremacist

“I will say then that I am not, nor ever have been in favor of bringing about in any way the social and political equality of the white and black races, that I am not nor ever have been in favor of making voters or jurors of Negroes, nor of qualifying them to hold office, nor to intermarry with white people . . . . I as much as any man am in favor of the superior position assigned to the white race.”

— Abraham Lincoln, First Lincoln-Douglas Debate, Ottawa, Illinois, Sept. 18, 1858, in The Collected Works of Abraham Lincoln vol.3, pp. 145-146.

Donald Sensing argues that the Civil War, for Lincoln, was about preserving the Union of these United States, not about abolishing slavery.

Donald also wrote: “The Confederate States of America was founded to do one thing only: to preserve the power of one class of people to literally own as chattel property another class of people. There is no other reason the CSA existed.

Cold Exposure May Help You Lose Weight

Well below room temp here

Should be well below room temp here

David Mendosa found a 2016 research report suggesting that cool temperatures may help with weight management by activating our brown fat, which burns more calories. Heat generated by brown fat is derived from glucose and triglycerides. Keep in mind as you read further that a comfortable environment temperature for a clothed human is about 23°C or 73°F. Those temps don’t stress our bodies by requiring us to either generate or dissipate extra body heat.

David writes:

Researchers have discovered that when we get mildly cold, which they define as being cool without shivering, our bodies burn more calories. As a result, managing our weight can be easier.
This is the conclusion of a recent review that two researchers at Maastricht University Medical Center in the Netherlands published in the November 2016 issue of the professional journal Diabetologia. The title of their article, “Combatting type 2 diabetes by turning up the heat,” puzzled me at first.

The title confused me because the study is about turning down the heat in the room we’re in. But then our bodies compensate by turning up their internal heat production.

When our body does this, its energy expenditure increases, ratcheting up our metabolism. Being mildly cold revs up our bodies’ brown fat, which unlike white fat, burns calories instead of storing them.

It’s not quite clear how much cold exposure it takes to turn on your brown fat. From the link above:

Cold acclimation by intermittent exposure to a cool (14–17°C) [57–63°F], or cold (10°C) [50°F] environment resulted in significant increases in NST [non-shivering thermogenesis or heat production] capacity. A 10 day cold acclimation study with 6 hour exposure to 14–15°C [57–59°F] per day was enough to significantly increase NST by 65% on average. A 6 week mild cold acclimation study (daily 2 hour cold exposure at 17°C [63°F]) also resulted in an increase in NST together with a concomitant decrease in body fat mass. The latter two studies also revealed significant increases in BAT [brown adipose tissue] presence and activation. All in all, cold-induced BAT activity is significant in adults and parallels NST. The actual quantitative contributions of BAT and of other tissues (e.g. skeletal muscle) to whole-body NST are, however, not elucidated and await further studies. Furthermore, more information is needed on the duration, timing and temperatures to find out which treatments are most effective with respect to increasing NST.

Furthermore, cold exposure over the course of 10 days increased insulin sensitivity in T2 diabetics by 43%. Eight study subjects, probably in the Netherlands, were exposed to temps of 14–15°C [57–59°F] but I don’t know for how many hours a day. Increased insulin sensitivity should help keep a lid on blood sugar levels and reduce the need for diabetes drugs.

In case you’re elderly, obese, or have type 2 diabetes, be aware that the activation of brown fat by cold exposure is not as robust as in others.

On the other hand, I found evidence that higher ambient temperatures (above 23°C) [73°F] may also help with weight management, regardless of what brown fat is doing.

Science is hard.

Steve Parker, M.D.

PS: Check out my books for more ideas on weight management.


Yes: You Can You Regain Muscle Mass After Age 60

She'll lose muscle fibers if she gets too sedentary as she ages

She’ll lose muscle fibers if she gets too sedentary as she ages

“Our lab and others have shown repeatedly that older muscles will grow and strengthen,” says Marcas Bamman, a professor of integrative biology at the University of Alabama at Birmingham. In his studies, men and women in their 60s and 70s who began supervised weight training developed muscles that were as large and strong as those of your average 40-year-old.”

Source: Can You Regain Muscle Mass After Age 60? – The New York Times

Dr. Bamman says older folks (over 60?) don’t add new muscle fibers like young’uns do. But an effective exercise program will cause hypertrophy (growth) of the existing muscle fibers. “Effectiveness” probably depends on exhausting muscle groups during weigh training.

Recipe: Rosemary Roasted Brussels Sprouts With Onion

Final product without Parmesan sprinkles. That's sous vide chicken in the foreground.

Final product without Parmesan sprinkles. That’s sous vide chicken in the foreground.

At my request, my wife bought me a mess o’ Brussels sprouts, and I’ve been experimenting with recipes.

Sprouts sliced in half

Sprouts sliced in half

Ingredients this time are the sprouts, dried rosemary (i.e., not fresh although it grows where I live), salt, pepper, extra virgin olive oil, fresh garlic, and diced onion.

FYI, rosemary is used as an ornamental landscaping plant in southern Arizona.

To promote release of flavor, I sautéed three garlic cloves and the rosemary in EVOO.

Releasing the flavors of garlic and rosemary over medium heat for perhaps 3 minutes

Releasing the flavors of garlic and rosemary over medium heat for perhaps 3 minutes

Then I sliced the sprouts in half along their long axis, to reduce cooking time. (Cut them so the leaves stay attached to the internal stalk.) You’d have to cut them in half before you eat ’em anyway.

I dumped all ingredients into a bowel and mixed thoroughly to ensure the sprouts were coated with oil.

Ready for the oven

Ready for the oven. I used about 3/4 cup of diced onion.

Everything except the bowl was transferred to a cooking sheet covered with aluminum foil (easy clean-up!), which I then popped into an oven pre-heated to 425°F. I cooked for 25 minutes. At around the 10 and 17-minute marks, I pulled the concoction out of the oven and stirred/flipped the ingredients to promote even cooking and browning. Your cooking time will vary from 17 to 25 minutes depending on your preferences. If you want some browning of the sprouts, you likely need to cook longer than 17 minutes. Unless your oven runs hotter than mine.

This is my favorite roasted Brussels sprouts recipe thus far. For an extra flavor zing, sprinkle with some Parmesan cheese just before eating. In the future, I may  top the ingredients with some other type of cheese a minute before the cooking is completed. Bacon bits are another tasty option.

Steve Parker, M.D.

Not "real" Parmesan from Italy. For example, this one contains cellulose "to prevent caking."

Not “real” Parmesan from the Parma region of Italy. For example, this one contains cellulose “to prevent caking.”