Category Archives: Health

Another study on dietary fat

From The Lancet:

 

Background

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.

Methods

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.

Interpretation

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.

 

and

 

Research in context

Evidence before this study

We did a systematic search in PubMed for relevant articles published between Jan 1, 1960, and May 1, 2017, restricted to the English language. Our search terms included “carbohydrate”, “total fat”, “saturated fatty acid”, “monounsaturated fatty acid”, “polyunsaturated fatty acid”, “total mortality”, and “cardiovascular disease”. We searched published articles by title and abstract to identify relevant studies. We also hand-searched reference lists of eligible studies. We considered studies if they evaluated association between macronutrient intake and total mortality or cardiovascular disease. The studies cited in this report are not an exhaustive list of existing research. Existing evidence on the associations of fats and carbohydrate intake with cardiovascular disease and mortality are mainly from North America and Europe.

Added value of this study

Current guidelines recommend a low fat diet (<30% of energy) and limiting saturated fatty acids to less than 10% of energy intake by replacing them with unsaturated fatty acids. The recommendation is based on findings from some North American and European countries where nutrition excess is of concern. It is not clear whether this can be extrapolated to other countries where undernutrition is common. Moreover, North American and European populations consume a lower carbohydrate diet than populations elsewhere where most people consume very high carbohydrate diets mainly from refined sources. Consistent with most data, but in contrast to dietary guidelines, we found fats, including saturated fatty acids, are not harmful and diets high in carbohydrate have adverse effects on total mortality. We did not observe any detrimental effect of higher fat intake on cardiovascular events. Our data across 18 countries adds to the large and growing body of evidence that increased fats are not associated with higher cardiovascular disease or mortality.

Implications of all the available evidence

Removing current restrictions on fat intake but limiting carbohydrate intake (when high) might improve health. Dietary guidelines might need to be reconsidered in light of consistent findings from the present study, especially in countries outside of Europe and North America.

The study appears mainly to have been funded by Canadian health organizations.

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Cancer Vaccine

This latest great report on a cancer cure comes from Stanford Medicine, which I consider a reputable source.

 

Injecting minute amounts of two immune-stimulating agents directly into solid tumors in mice can eliminate all traces of cancer in the animals, including distant, untreated metastases, according to a study by researchers at the Stanford University School of Medicine.

The approach works for many different types of cancers, including those that arise spontaneously, the study found.

The researchers believe the local application of very small amounts of the agents could serve as a rapid and relatively inexpensive cancer therapy that is unlikely to cause the adverse side effects often seen with bodywide immune stimulation.

“When we use these two agents together, we see the elimination of tumors all over the body,” said Ronald Levy, MD, professor of oncology. “This approach bypasses the need to identify tumor-specific immune targets and doesn’t require wholesale activation of the immune system or customization of a patient’s immune cells.”

One agent is currently already approved for use in humans; the other has been tested for human use in several unrelated clinical trials. A clinical trial was launched in January to test the effect of the treatment in patients with lymphoma.

Here’s how it works:

Levy’s method works to reactivate the cancer-specific T cells by injecting microgram amounts of two agents directly into the tumor site. (A microgram is one-millionth of a gram). One, a short stretch of DNA called a CpG oligonucleotide, works with other nearby immune cells to amplify the expression of an activating receptor called OX40 on the surface of the T cells. The other, an antibody that binds to OX40, activates the T cells to lead the charge against the cancer cells. Because the two agents are injected directly into the tumor, only T cells that have infiltrated it are activated. In effect, these T cells are “prescreened” by the body to recognize only cancer-specific proteins.

Some of these tumor-specific, activated T cells then leave the original tumor to find and destroy other identical tumors throughout the body.

The approach worked startlingly well in laboratory mice with transplanted mouse lymphoma tumors in two sites on their bodies. Injecting one tumor site with the two agents caused the regression not just of the treated tumor, but also of the second, untreated tumor. In this way, 87 of 90 mice were cured of the cancer. Although the cancer recurred in three of the mice, the tumors again regressed after a second treatment. The researchers saw similar results in mice bearing breast, colon and melanoma tumors.

“I don’t think there’s a limit to the type of tumor we could potentially treat, as long as it has been infiltrated by the immune system.”

Mice genetically engineered to spontaneously develop breast cancers in all 10 of their mammary pads also responded to the treatment. Treating the first tumor that arose often prevented the occurrence of future tumors and significantly increased the animals’ life span, the researchers found.

Finally, Sagiv-Barfi explored the specificity of the T cells by transplanting two types of tumors into the mice. She transplanted the same lymphoma cancer cells in two locations, and she transplanted a colon cancer cell line in a third location. Treatment of one of the lymphoma sites caused the regression of both lymphoma tumors but did not affect the growth of the colon cancer cells.

“This is a very targeted approach,” Levy said. “Only the tumor that shares the protein targets displayed by the treated site is affected. We’re attacking specific targets without having to identify exactly what proteins the T cells are recognizing.”

So we can’t all go get a shot and never get cancer.  But if a tumor is detected, and this works out in trials, we could get a shot and all of that type of cancer within our body would be killed by our own T cells.  If we got some other cancer, we would have to go get another shot for that one.

 

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Gut Biome and Exercise

From New York Times:

(Researchers) began by recruiting 32 men and women who did not exercise. About half were obese and the rest of normal weight.

The scientists took blood and fecal samples and tested everyone’s aerobic fitness. Then they had the men and women begin supervised workouts, during which their efforts increased over time from about 30 minutes of easy walking or cycling to about an hour of vigorous jogging or pedaling three times per week.

The volunteers were asked not to change their normal diets.

After six weeks, the scientists collected more samples and retested everyone, and then asked the volunteers to stop exercising altogether.

Six weeks later, the tests were once again repeated.

The subsequent analysis showed that the volunteers’ gut bugs had changed throughout the experiment, with some increasing in numbers and others declining. The researchers also found changes in the operations of many microbes’ genes. Some of those genes were working harder now, while others had grown silent.

Most of these changes were not shared from one person to the next. Everyone’s gut responded uniquely to exercise.

But there were some similarities, the researchers found. In particular, they noted widespread increases in certain microbes that can help to produce substances called short-chain fatty acids. These fatty acids are believed to aid in reducing inflammation in the gut and the rest of the body. They also work to fight insulin resistance, a precursor to diabetes, and otherwise bolster our metabolisms.

Most of the volunteers had larger concentrations of these short-chain fatty acids in their intestines after exercise, along with the microbes that produce them.

These increases were greatest, though, among the volunteers who had begun the experiment lean compared to those who were obese, the scientists found.

And perhaps not surprisingly, almost all of the changes in people’s guts dissipated after six weeks of not exercising. By and large, their microbiomes reverted to what they had been at the study’s start.

Still, the study’s overall results suggest that even a few weeks of exercise can alter the makeup and function of people’s microbiomes, says Jeffrey Woods, a professor of kinesiology and community health at the University of Illinois who conducted the study, along with his doctoral student Jacob Allen (now a postdoctoral researcher at Ohio State University) and others.

In theory, Dr. Woods continues, these changes could contribute to some of the broader health benefits of exercise, such as its ability to reduce inflammation throughout the body.

“But more studies need to be done to prove this,” he says.

This is really interesting because it gives a physical reason for why exercise helps reduce diabetes.  Also more info on the biome.

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Vaccines and why the anecdotes?

Just saw this paper dated 2008 from NIH titled  “Genetics and the myth of vaccine encephalopathy”

It talks about the anecdotes of children receiving vaccines and then within one to 14 days, seemingly regressing and becoming autistic.  It turns out there is an explanation for this:  Vaccines can cause fevers.  A very small number of people have either genetic defects/mutations (which happen during development – not inherited) or mitochondrial disorders.  These already existing issues lead to autism, triggered by a fever.  So the person would have become autistic when triggered by a fever, whether that fever was caused by a vaccine or some other (inevitable) cause.

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Insulin – Illness Connection

From Mark’s Daily Apple

Hyperglycemia

If you’re insulin resistant, insulin doesn’t work very well. You need more of it to get the same effect an insulin sensitive person would get. When insulin doesn’t work, its ability to shuttle glucose out of the blood suffers, and blood glucose goes up and stays up. That’s hyperglycemia. Everyone “knows” that high blood sugar is bad, but why? What exactly goes wrong?

Some cells are passive recipients of blood sugar, while others have mechanisms that prevent excess blood sugar from entering their membranes. In the presence of high blood sugar, the passive recipients begin producing excessive amounts of reactive oxygen species (ROS). ROS aren’t pathological in and of themselves. They’re signaling molecules that our bodies need for healthy cellular function. But unchecked ROS generation induced by hyperglycemia causes a lot of problems.

In endothelial cells, hyperglycemia inhibits the production of nitric oxide. Nitric oxide is a vasodilator—it helps our blood vessels widen to accommodate increased blood flow and reduce shear stress. Without sufficient nitric oxide, our blood vessels are more susceptible to high blood pressure and our risk for heart disease and atherosclerosis goes up.

In neurons, hyperglycemia causes shrinkage. No one likes shrinkage, especially not in the brain cells where thinking occurs.

In pancreatic beta cells, hyperglycemia reduces cell mass, induces oxidative stress, and reduces functionality. Since the pancreas secretes insulin—the stuff used to deal with excess blood glucose—this is disastrous.

Cancer

Insulin is a growth promoting agent, and cancer is a disease of unchecked cellular growth. There are nuances to this of course. But by and large, those are true statements. It’s no surprise that hyperinsulinemia is a risk factor for most, if not all cancers.

While insulin isn’t everything when it comes to cancer, the links are undeniable and myriad—and worrying.

The link between colon cancer and hyperinsulinemia likely involves the increased availability of insulin-like growth factor in a hyperinsulinemic state. Post-menopausal women with genetic variants related to insulin resistance and hyperinsulinemia have a greater risk of colorectal cancer, and colon cancer patients who eat the most insulinogenic foods have poorer outcomes.

In breast cancer, hyperglycemia increases the tumors’ resistance to chemotherapy. Fixing the hyperglycemia makes chemotherapy more effective.

People with a genetic predisposition toward hyperinsulinemia have a higher chance of developing pancreatic cancer.

Independent of bodyweight, hyperinsulinemia predicts endometrial cancer; so does a high postprandial insulin response.

Diabetics who use insulin therapy have an increased risk of liver cancer.  One study of Taiwanese diabetics found that those on insulin therapy have an elevated risk of dying from cancer and from non-cancer.

Across the board, in both obese and people of normal bodyweight, hyperinsulinemia, whether it’s genetic, simulated, or diet-driven, increases cancer incidence and mortality. 

Okay, okay. That’s all rather convincing, but there’s a chance that these are merely associations and some common factor is causing both the hyperinsulinemia/insulin resistance and the cancer. Right?

What seems to counter that hypothesis is the effect of metformin, an anti-diabetic drug, on cancer. Compared to other diabetic drugs, metformin reduces the risk of cancer in type 2 diabetics. Metformin’s mechanism of action? A reduction in insulin levels and improvement of insulin resistance.

Alzheimer’s Disease

Alzheimer’s hits families like a freight train, but if you know what to look for you can see it coming.

Alzheimer’s and other forms of dementia are characterized by brain insulin resistance. In experiments where researchers simulate brain diabetes by administering drugs known to induce brain insulin resistance, it looks almost exactly like Alzheimer’s. Some people even call Alzheimer’s type 3 diabetes, so closely is it linked to insulin resistance.

Alzheimer’s patients have high blood sugar, but their neurons are so resistant to the effects of insulin that they’re unable to utilize the available glucose for energy. That’s why ketogenic diets and ketones in particular are so helpful for Alzheimer’s; they offer an alternative fuel source that even the insulin resistant brain can utilize.

Heart Disease

Independent of most other factors, insulin resistance predicts heart disease riskOne of the best predictors of heart disease risk—the HDL:triglyceride ratio—also happens to be an accurate barometer of insulin resistance. The lower your HDL and the higher your triglycerides, the more likely you are to be insulin resistant.

The two go hand in hand, and it’s not just a coincidence.

As you saw in the hyperglycemia section, insulin resistance can increase the risk of heart disease by increasing hyperglycemia and reducing endothelial function. This impairs the blood vessels’ ability to react to stressors and makes them more vulnerable to atherosclerosis.

What You Can Do

A big step, maybe the first step when you’re insulin resistant with hyperinsulinemia, or even just suspect you are, is to reduce your intake of the most insulinogenic macronutrient around: carbs. This stems the tide and stops feeding the fire until you can figure out and resolve the root cause of your dysfunction.

That next part is harder. Some of it is genetic; there will be people who simply make more insulin than others, or who are more insulin resistant as a baseline. Oftentimes the dysfunction is multifactorial, stemming from a dozen different causes, all of which require your attention. In past posts, I’ve explained strategies for combating insulin resistance and reducing hyperinsulinemia. If you haven’t read those yet, do so.

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Best of 2017 from Mark’s Daily Apple

From Mark’s Daily Apple:

1. Vegetable oils are still really, really bad.

2. Keto works.

3. Everything has a circadian rhythm, and the circadian rhythm affects everything.

4. What the Health, this year’s token vegan screed, came out to rapturous applause. In one of my favorite pieces of the year, Robb Wolf took it apart piece by piece and, in doing so, definitively commented on anti-meat hysteria and bad science in general.

5. We learned that the sugar industry has been stifling anti-sugar research results for decades, surprising no one while enraging almost everyone (with an honest bone in their body).

6. We learned more and more about ancient human evolution and migration. It turns out that our history is even crazier and more impressive than we thought.

7. Human gene editing drew ever nearer to the mainstream.

8. Awareness of digital media’s effect on our health and happiness grew.

9. There was serious debate over whether we’re educating and parenting our kids the right way.

10. Even as health and food-related tech has largely come up short, there were some promising developments.

 

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Neuroscience & Module Model

From Eric Barker:

Both neuroscience and psychology are starting to agree. Sometimes you don’t act like you because there is no singular “you.”

Here’s noted science author Robert Wright:

In this view, your mind is composed of lots of specialized modules—modules for sizing up situations and reacting to them—and it’s the interplay among these modules that shapes your behavior. And much of this interplay happens without conscious awareness on your part. The modular model of the mind, though still young and not fully fleshed out, holds a lot of promise. For starters, it makes sense in terms of evolution: the mind got built bit by bit, chunk by chunk, and as our species encountered new challenges, new chunks would have been added. As we’ll see, this model also helps make sense of some of life’s great internal conflicts, such as whether to cheat on your spouse, whether to take addictive drugs, and whether to eat another powdered-sugar doughnut.

Now modules aren’t physical structures in the brain, just like apps aren’t hardware in your phone. They’re software; the human nature algorithms that Mother Nature coded over thousands of generations of evolution.

Whichever module has the most emotional kick attached to it at any point wins the competition to be “you.”

Buddhism recognized this problem over 1000 years ago. And it also came up with a solution: mindfulness meditation.

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