Low Carb Diets Found to Feed Heart Disease

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People going on low carb diets may not see a rise in their cholesterol levels. How is that possible? Because weight loss by any means can drop our cholesterol. We could go on an all-Twinkie diet and lower our cholesterol as long as we didn't eat too many. A good cocaine habit could do it. Anything that drops our weight can drop our cholesterol, but the goal isn't to fit into a skinnier casket; the reason we care about cardiovascular risk factors like cholesterol is because we care about cardiovascular risk, the health of our arteries.

Now we have studies that measure the impact of low carb diets on arteries directly, and a review of all the best studies to date found that low-carb diets impair arterial function, as evidenced by a decrease in flow-mediated dilation, meaning low-carb diets effectively stiffen people's arteries. And since that meta-analysis was published, a new study found the same thing: "A dietary pattern characterized by high protein and fat, but low carbohydrate was associated with poorer peripheral small artery function," again measuring blood flow into people's limbs. But peripheral circulation is not as important as the circulation in the coronary arteries that feed our heart.

There has only been one study ever done measuring actual blood flow to the heart muscles of people eating low-carb diets. Dr. Richard Fleming, an accomplished nuclear cardiologist, enrolled 26 people into a comprehensive study of the effects of diet on cardiac function using the latest in nuclear imaging technology-so-called SPECT scans, enabling him to actually directly measure the blood flow within the coronary arteries.

He then put them all on a healthy vegetarian diet, and a year later the scans were repeated. By that time, however, ten of the patients had jumped ship onto the low carb bandwagon. At first I bet he was disappointed, but surely soon realized he had an unparalleled research opportunity dropped into his lap. Here he had extensive imaging of ten people before and after following a low carb diet and 16 following a high carb diet. What would their hearts look like at the end of the year? We can talk about risk factors all we want, but compared to the veg group, did the coronary heart disease of the patients following the Atkins-like diets improve, worsen, or stay the same?

Those sticking to the vegetarian diet showed a reversal of their heart disease as expected. Their partially clogged arteries literally got cleaned out. They had 20% less atherosclerotic plaque in their arteries at the end of the year than at the beginning. What happened to those who abandoned the treatment diet, and switched over to the low-carb diet? Their condition significantly worsened. 40% to 50% more artery clogging at the end of the year. In heart scans of the patients, as seen in my video, Low Carb Diets and Coronary Blood Flow, the yellow and particularly red areas represent blood flow through the coronary arteries to the heart muscle. The scan of one of the patients who went on a plant-based diet, shows how their arteries opened right up increasing the blood flow. Another person, however, started out with good flow, but after a year on a low-carb diet, they significantly clogged down their arterial blood flow.

So this is the best science we have, demonstrating the threat of low-carb diets, not just measuring risk factors, but actual blood flow in people's hearts on different diets. Of course the reason we care about cardiac blood flow, is we don't want to die. Another meta-analysis was recently published that finally went ahead and measured the ultimate end-point, death, and low-carb diets were associated with a significantly higher risk of all-cause mortality, meaning living a significantly shorter lifespan.

The reason I have so few videos about low-carb diets is that I already wrote a book about it. Carbophobia is now available free online full-text at AtkinsFacts.org. Atkins' lawyers threatened to sue, leading to a heated exchange you're sure to enjoy that I reprint in the book. I did touch on it Atkins Diet: Trouble Keeping it Up, though low carb diets don't necessarily have to be that unhealthy (see my video Plant-Based Atkins Diet).

Here are some videos I've done on conquering our #1 killer:

-Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day, and From Table to Able.

Image Credit: ryan.dowd / Flickr

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How Fatty Foods May Affect Our Love Life

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The food industry, like the tobacco companies and other drug lords, has been able to come up with products that tap into the same dopamine reward system that keeps people smoking cigarettes, using marijuana, and eating candy bars (See Are Sugary Foods Addictive?). New research, highlighted in my video Are Fatty Foods Addictive? suggests that fat may have similar effects on the brain. If people are fed yogurt packed with butter fat, within 30 minutes they exhibit the same brain activity as those who just drank sugar water.

People who regularly eat ice cream (sugar and fat) have a deadened dopamine response in their brains in response to drinking a milkshake. It's similar to when drug abusers have to use more and more to get the same high. Frequent ice cream consumption "is related to a reduction in reward-region (pleasure center) responsivity in humans, paralleling the tolerance observed in drug addiction." Once we've so dulled our dopamine response, we may subsequently overeat in an effort to achieve the degree of satisfaction experienced previously, contributing to unhealthy weight gain.

What do fatty and sugary foods have in common? They are energy-dense. It may be less about the number of calories than their concentration. Consumption of a calorie-dilute diet doesn't lead to deadened dopamine responsivity, but a calorie-dense diet with the same number of calories does. It's like the difference between cocaine and crack: same stuff chemically, but by smoking crack cocaine we can deliver a higher dose quicker to our brain.

As an aside, I found it interesting that the control drink in these milkshake studies wasn't just water. They can't use water because our brain actually tastes water on the tongue (who knew!). So instead the researchers had people drink a solution "designed to mimic the natural taste of saliva." Ew!

Anyway, with this new understanding of the neural correlates of food addiction, there have been calls to include obesity as an official mental disorder. After all, both obesity and addiction share the inability to restrain behavior in spite of an awareness of detrimental health consequences, one of the defining criteria of substance abuse. We keep putting crap in our bodies despite the knowledge that we have a problem that is likely caused by the crap, yet we can't stop (a phenomena called the "pleasure trap").

Redefining obesity as an addiction, a psychiatric disease, would be a boon to the drug companies that are already working on a whole bunch of drugs to muck with our brain chemistry. For example, subjects given an opiate blocker (like what's done for people with heroin overdoses to block the effects of the drug) eat significantly less cheese -- it just doesn't do as much for them anymore when their opiate receptors are blocked.

Rather than taking drugs, though, we can prevent the deadening of our pleasure center in the first place by sticking to foods that are naturally calorically dilute, like whole plant foods. This can help bring back our dopamine sensitivity such that we can again derive the same pleasure from the simplest of foods (see Changing Our Taste Buds). And this is not just for people who are obese. When we regularly eat calorie dense animal and junk foods like ice cream, we can blunt our pleasure so that we may overeat to compensate. When our brain down-regulates dopamine receptors to deal with all these jolts of fat and sugar, we may experience less enjoyment from other activities as well.

That's why cocaine addicts may have an impaired neurological capacity to enjoy sex, and why smokers have an impaired ability to respond to positive stimuli. Since these all involve the same dopamine pathways, what we put into our body--what we eat--can affect how we experience all of life's pleasures.

So to live life to the fullest, what should we do? The food industry, according to some addiction specialists, "should be given incentives to develop low calorie foods that are more attractive, palatable and affordable so that people can adhere to diet programs for a long time." No need! Mother Nature beat them to it--that's what the produce aisle is for.

By starting to eat healthfully, we can actually change how things taste. Healthiest means whole plant foods, which tend to be naturally dilute given their water and fiber content. Not only is fiber also calorie-free, but one might think of it as having "negative" calories, given the fermentation of fiber in our bowel into anti-obesity compounds (as well as anti-inflammatory, anti-cancer compounds). For this reason, those eating plant-based diets eat hundreds of fewer calories without even trying. (See my video Nutrient-Dense Approach to Weight Management).

-Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day, and From Table to Able.

Images thanks to Burger Austin / Flickr

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Can One Become a Sugar Addict?

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People have chewed coca leaves for at least 8,000 years as a mild stimulant without any evidence of addiction, but when certain components are isolated and concentrated into cocaine, we've got a problem. The same may be true of sugar--people don't tend to binge on bananas. The isolation of sugar from the whole food may be the reason we're more likely to supersize soda than sweet potatoes, or why we're less likely to eat too much corn on the cob, but can't seem to get enough high fructose corn syrup.

The overconsumption of sugar-sweetened diets has often been compared to drug addiction. However, until very recently this parallel was based more on anecdotal evidence than on solid scientific grounds. But now we have PET scans, imaging technology that can measure brain activity. It all started with a publication from the Institute of Clinical Physiology that showed decreased dopamine sensitivity in obese individuals. The heavier they were, the less responsive to dopamine they appeared to be. We see the same reduction in sensitivity in cocaine addicts and alcoholics, which "would suggest that a reduction in dopamine receptors is associated with addictive behavior irrespective of whether it is due to food or to addictive drugs, as seen in substance abusers."

Dopamine is considered the neurotransmitter primarily involved in the pleasure and reward center of our brain, helping to motivate our drive for things like food, water and sex--all necessary for the perpetuation of our species. It was healthy and adaptive for our primate brains to drive us to eat that banana when there wasn't much food around. But now that fruit is in fruit loop form, this adaptation has "become a dangerous liability." The original Coca-Cola formulation actually included coca leaf, but now, perhaps, its sugar content may be the addictive stand-in.

What about artificial sweeteners? Though some are less harmful than others (Erythritol May Be a Sweet Antioxidant as opposed to Aspartame-Induced Fibromyalgia), they could still have adverse effects regardless of their individual chemistry. See my 3-part series:

  1. How Diet Soda Could Make Us Gain Weight
  2. Neurobiology of Artificial Sweeteners
  3. Unsweetening the Diet

What about fatty foods like meat? Does fat have addictive qualities as well? Good question! Check out my video Are Fatty Foods Addictive?

-Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day, and From Table to Able.

Images thanks to MattysFlicks / Flickr

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Can We Fight the Blues With Greens?









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Why does frequent consumption of vegetables appear to cut one’s odds of depression by more than half? And "frequent" was defined as eating vegetables not 3 or more times a day, but just 3 or more times a week.

A 2012 study was found that eliminating animal products improved mood within two weeks. The researchers blamed arachidonic acid, found primarily in chicken and eggs, which might adversely impact mental health via a cascade of brain inflammation. More on this inflammatory omega-6 fatty acid in:

But better moods on plant-based diets could also be from the good stuff in plants—a class of phytonutrients that cross the blood brain barrier into our heads. A recent review in the journal, Nutritional Neuroscience, suggests that eating lots of fruits and vegetables “may present a noninvasive natural and inexpensive therapeutic means to support a healthy brain.” But how?

To understand the latest research, we need to understand the underlying biology of depression—the so-called monoamine theory of depression. It's the idea that depression may arise out of a chemical imbalance in the brain. In my video Fighting the Blues with Greens? I run through an oversimplified version.

One of the ways the billions of nerves in our brain communicate with one another is through chemical signals called neurotransmitters. Two nerve cells don’t actually touch—there’s a physical gap between them. To bridge that gap, when one nerve wants to tap the other on the shoulder it releases chemicals into that gap, including three monoamines: serotonin, dopamine and norepinephrine. These neurotransmitters then float over to the other nerve to get its attention. The first nerve then sucks them back in to be reused the next time it wants to talk. It’s also constantly manufacturing more monoamines, and an enzyme, monoamine oxidase, is constantly chewing them up to maintain just the right amount.

The way cocaine works is by acting as a monoamine re-uptake inhibitor. It blocks the first nerve from sucking back up these three chemicals and so there’s a constant tapping on the shoulder—constant signaling—to the next cell. Amphetamines work in the same way but also increase the release of monoamines. Ecstasy works like speed, but just causes comparatively more serotonin release.

After awhile, the next nerve may say “enough already!” and down-regulate its receptors to turn down the volume. It puts in earplugs. So we need more and more of the drug to get the same effect, and then when we’re not on the drug we may feel crappy because normal volume transmission just isn’t getting through.

Antidepressants are thought to work along similar mechanisms. People who are depressed appear to have elevated levels of monoamine oxidase in their brain. That’s the enzyme that breaks down those neurotransmitters. In the video mentioned previously, I show the levels of monoamine oxidase in the brains of depressed individuals versus healthy individuals. If the levels of our neurotransmitter-eating enzyme is elevated, then our levels of neurotransmitters drops, and we become depressed (or so the theory goes).

So a number of different classes of drugs have been developed. The tricyclic antidepressants, named because they have three rings like a tricycle, appear to block norepinephrine and dopamine re-uptake, and so even though our enzymes may be eating these up at an accelerated rate, what gets released sticks around longer. Then there were the SSRIs (the selective serotonin reuptake inhibitors) like Prozac. Now we know what that means—they just block the re-uptake of serotonin. Then there are drugs that just block the re-uptake of norepinephrine, or block dopamine re-uptake, or a combination. But if the problem is too high levels of monoamine oxidase, why not just block the enzyme? Make a monoamine oxidase inhibitor. They did, but monoamine oxidase inhibitors are considered drugs of last resort because of serious side effects—not the least of which is the dreaded “cheese effect,” where eating certain foods while on the drug can have potentially fatal consequences. If only there was a way to dampen the activity of this enzyme without the whole bleed-into-our-brain-and-die thing.

Now we can finally talk about the latest theory as to why fruits and vegetables may improve our mood. There are inhibitors of the depression-associated enzyme in various plants. There are phytonutrients in spices, such as clove, oregano, cinnamon, and nutmeg, that inhibit monoamine oxidase, but people don’t eat enough spices to get enough into the brain. A certain dark green leafy has a lot, but its name is tobacco, which may actually be one of the reasons cigarettes make smokers feel so good. OK, but what if we don’t want brain bleeds or lung cancer? Well, there is a phytonutrient found in apples, berries, grapes, kale, onions, and green tea that may indeed affect our brain biology enough to improve our mood, which may help explain why those eating plant-based diets tend to have superior mental health.

For other natural treatments for mental illness, check out:

-Michael Greger, M.D.

If you haven’t yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death and More Than an Apple a Day.

Image credit: liz west / Flickr

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