Are Sugar Pills Better than Antidepressant Drugs?

Do Antidepressant Drugs Really Work.jpg

We've learned that exercise compares favorably to antidepressant medications as a first-line treatment for mild to moderate depression (in my video Exercise vs. Drugs for Depression). But how much is that really saying? How effective are antidepressant drugs in the first place?

A recent meta-analysis sparked huge scientific and public controversy by stating that the placebo effect can explain the apparent clinical benefits of antidepressants. But aren't there thousands of clinical trials providing compelling evidence for antidepressant effectiveness? If a meta-analysis compiles together all the best published research, how could it say they don't work much better than sugar pills?

The key word is "published."

What if a drug company decided only to publish studies that showed a positive effect, but quietly shelved and concealed any studies showing the drug didn't work? If you didn't know any better, you'd look at the published medical literature and think "Wow, this drug is great." And what if all the drug companies did that? To find out if this was the case, researchers applied to the FDA under the Freedom of Information Act to get access to the published and unpublished studies submitted by pharmaceutical companies, and what they found was shocking.

According to the published literature, the results of nearly all the trials of antidepressants were positive, meaning they worked. In contrast, FDA analysis of the trial data showed only roughly half of the trials had positive results. In other words, about half the studies showed the drugs didn't work. Thus, when published and unpublished data are combined, they fail to show a clinically significant advantage for antidepressant medication over a sugar pill. Not publishing negative results undermines evidence-based medicine and puts millions of patients at risk for using ineffective or unsafe drugs, and this was the case with these antidepressant drugs.

These revelations hit first in 2008. Prozac, Serzone, Paxil and Effexor worked, but so did sugar pills, and the difference between the drug and placebo was small. That was 2008. Where were we by 2014? Analyses of the published data and the unpublished data that were hidden by drug companies reveals that most (if not all) of the benefits of antidepressants are due to the placebo effect. And what's even worse, Freedom of Information Act documents show the FDA knew about it but made an explicit decision to keep this information from the public and from prescribing physicians.

How could drug companies get away with this?

The pharmaceutical industry is considered the most profitable and politically influential industry in the United States, and mental illness can be thought of as the drug industry's golden goose: incurable, common, long term and involving multiple medications. Antidepressant medications are prescribed to 8.7 percent of the U.S. population. It's a multi-billion dollar market.

To summarize, there is a strong therapeutic response to antidepressant medication; it's just that the response to placebo is almost as strong. Indeed, antidepressants offer substantial benefits to millions of people suffering from depression, and to cast them as ineffective is inaccurate. Just because they may not work better than fake pills doesn't mean they don't work. It's like homeopathy--just because it doesn't work better than the sugar pills, doesn't mean that homeopathy doesn't work. The placebo effect is real and powerful.

In one psychopharmacology journal, a psychiatrist funded by the Prozac company defends the drugs stating, "A key issue is disregarded by the naysaying critics. If the patient is benefiting from antidepressant treatment does it matter whether this is being achieved via drug or placebo effects?"

Of course it matters!

Among the side effects of antidepressants are: sexual dysfunction in up to three quarters of people, long-term weight gain, insomnia, nausea and diarrhea. About one in five show withdrawal symptoms when they try to quit. And perhaps more tragically, the drugs may make people more likely to become depressed in the future. Let me say that again: People are more likely to become depressed after treatment by antidepressants than after treatment by other means - including placebo.

So if doctors are willing to give patients placebo-equivalent treatments, maybe it'd be better for them to just lie to patients and give them actual sugar pills. Yes, that involves deception, but isn't that preferable than deception with a side of side effects? See more on this in my video Do Antidepressant Drugs Really Work?

If different treatments are equally effective, then choice should be based on risk and harm, and of all of the available treatments, antidepressant drugs may be among the riskiest and most harmful. If they are to be used at all, it should be as a last resort, when depression is extremely severe and all other treatment alternatives have been tried and failed.

Antidepressants may not work better than placebo for mild and moderate depression, but for very severe depression, the drugs do beat out sugar pills. But that's just a small fraction of the people taking these drugs. That means that the vast majority of depressed patients--as many as nine out of ten--are being prescribed medications that have negligible benefits to them.

Too many doctors quickly decide upon a depression diagnosis without necessarily listening to what the patient has to say and end up putting them on antidepressants without considering alternatives. And fortunately, there are effective alternatives. Physical exercise, for example can have lasting effects, and if that turns out to also be a placebo effect, it is at least a placebo with an enviable list of side effects. Whereas side effects of antidepressants include things like sexual dysfunction and insomnia, side effects of exercise include enhanced libido, better sleep, decreased body fat, improved muscle tone and a longer life.


There are other ways meta-analyses can be misleading. See The Saturated Fat Studies: Buttering Up the Public and The Saturated Fat Studies: Set Up to Fail.

More on the ethical challenges facing doctors and whether or not to prescribe sugar pills in The Lie That Heals: Should Doctors Give Placebos?

I've used the Freedom of Information Act myself to get access to behind the scenes industry shenanigans. See, for example, what I found out about the egg industry in Who Says Eggs Aren't Healthy or Safe? and Eggs and Cholesterol: Patently False and Misleading Claims.

This isn't the only case of the medical profession overselling the benefits of drugs. See How Smoking in 1956 is Like Eating in 2016, The Actual Benefit of Diet vs. Drugs and Why Prevention is Worth a Ton of Cure (though if you're worried about your mood they might make you even more depressed!)

In health,

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:

Image Credit: GraphicStock. This image has been modified.

Original Link

Are Sugar Pills Better than Antidepressant Drugs?

Do Antidepressant Drugs Really Work.jpg

We've learned that exercise compares favorably to antidepressant medications as a first-line treatment for mild to moderate depression (in my video Exercise vs. Drugs for Depression). But how much is that really saying? How effective are antidepressant drugs in the first place?

A recent meta-analysis sparked huge scientific and public controversy by stating that the placebo effect can explain the apparent clinical benefits of antidepressants. But aren't there thousands of clinical trials providing compelling evidence for antidepressant effectiveness? If a meta-analysis compiles together all the best published research, how could it say they don't work much better than sugar pills?

The key word is "published."

What if a drug company decided only to publish studies that showed a positive effect, but quietly shelved and concealed any studies showing the drug didn't work? If you didn't know any better, you'd look at the published medical literature and think "Wow, this drug is great." And what if all the drug companies did that? To find out if this was the case, researchers applied to the FDA under the Freedom of Information Act to get access to the published and unpublished studies submitted by pharmaceutical companies, and what they found was shocking.

According to the published literature, the results of nearly all the trials of antidepressants were positive, meaning they worked. In contrast, FDA analysis of the trial data showed only roughly half of the trials had positive results. In other words, about half the studies showed the drugs didn't work. Thus, when published and unpublished data are combined, they fail to show a clinically significant advantage for antidepressant medication over a sugar pill. Not publishing negative results undermines evidence-based medicine and puts millions of patients at risk for using ineffective or unsafe drugs, and this was the case with these antidepressant drugs.

These revelations hit first in 2008. Prozac, Serzone, Paxil and Effexor worked, but so did sugar pills, and the difference between the drug and placebo was small. That was 2008. Where were we by 2014? Analyses of the published data and the unpublished data that were hidden by drug companies reveals that most (if not all) of the benefits of antidepressants are due to the placebo effect. And what's even worse, Freedom of Information Act documents show the FDA knew about it but made an explicit decision to keep this information from the public and from prescribing physicians.

How could drug companies get away with this?

The pharmaceutical industry is considered the most profitable and politically influential industry in the United States, and mental illness can be thought of as the drug industry's golden goose: incurable, common, long term and involving multiple medications. Antidepressant medications are prescribed to 8.7 percent of the U.S. population. It's a multi-billion dollar market.

To summarize, there is a strong therapeutic response to antidepressant medication; it's just that the response to placebo is almost as strong. Indeed, antidepressants offer substantial benefits to millions of people suffering from depression, and to cast them as ineffective is inaccurate. Just because they may not work better than fake pills doesn't mean they don't work. It's like homeopathy--just because it doesn't work better than the sugar pills, doesn't mean that homeopathy doesn't work. The placebo effect is real and powerful.

In one psychopharmacology journal, a psychiatrist funded by the Prozac company defends the drugs stating, "A key issue is disregarded by the naysaying critics. If the patient is benefiting from antidepressant treatment does it matter whether this is being achieved via drug or placebo effects?"

Of course it matters!

Among the side effects of antidepressants are: sexual dysfunction in up to three quarters of people, long-term weight gain, insomnia, nausea and diarrhea. About one in five show withdrawal symptoms when they try to quit. And perhaps more tragically, the drugs may make people more likely to become depressed in the future. Let me say that again: People are more likely to become depressed after treatment by antidepressants than after treatment by other means - including placebo.

So if doctors are willing to give patients placebo-equivalent treatments, maybe it'd be better for them to just lie to patients and give them actual sugar pills. Yes, that involves deception, but isn't that preferable than deception with a side of side effects? See more on this in my video Do Antidepressant Drugs Really Work?

If different treatments are equally effective, then choice should be based on risk and harm, and of all of the available treatments, antidepressant drugs may be among the riskiest and most harmful. If they are to be used at all, it should be as a last resort, when depression is extremely severe and all other treatment alternatives have been tried and failed.

Antidepressants may not work better than placebo for mild and moderate depression, but for very severe depression, the drugs do beat out sugar pills. But that's just a small fraction of the people taking these drugs. That means that the vast majority of depressed patients--as many as nine out of ten--are being prescribed medications that have negligible benefits to them.

Too many doctors quickly decide upon a depression diagnosis without necessarily listening to what the patient has to say and end up putting them on antidepressants without considering alternatives. And fortunately, there are effective alternatives. Physical exercise, for example can have lasting effects, and if that turns out to also be a placebo effect, it is at least a placebo with an enviable list of side effects. Whereas side effects of antidepressants include things like sexual dysfunction and insomnia, side effects of exercise include enhanced libido, better sleep, decreased body fat, improved muscle tone and a longer life.


There are other ways meta-analyses can be misleading. See The Saturated Fat Studies: Buttering Up the Public and The Saturated Fat Studies: Set Up to Fail.

More on the ethical challenges facing doctors and whether or not to prescribe sugar pills in The Lie That Heals: Should Doctors Give Placebos?

I've used the Freedom of Information Act myself to get access to behind the scenes industry shenanigans. See, for example, what I found out about the egg industry in Who Says Eggs Aren't Healthy or Safe? and Eggs and Cholesterol: Patently False and Misleading Claims.

This isn't the only case of the medical profession overselling the benefits of drugs. See How Smoking in 1956 is Like Eating in 2016, The Actual Benefit of Diet vs. Drugs and Why Prevention is Worth a Ton of Cure (though if you're worried about your mood they might make you even more depressed!)

In health,

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:

Image Credit: GraphicStock. This image has been modified.

Original Link

Lipotoxicity: How Saturated Fat Raises Blood Sugar

NF-Nov24 Lipotoxicity How Saturated Fat Raises Blood Sugar copy.jpg

The reason those eating plant-based diets have less fat buildup in their muscle cells and less insulin resistance may be because saturated fats appear to impair blood sugar control the most.

The association between fat and insulin resistance is now widely accepted. Insulin resistance is due to so-called ectopic fat accumulation, the buildup of fat in places it's not supposed to be, like within our muscle cells. But not all fats affect the muscles the same. The type of fat, saturated vs. unsaturated, is critical. Saturated fats like palmitate, found mostly in meat, dairy and eggs, cause insulin resistance, but oleate, found mostly in nuts, olives and avocados may actually improve insulin sensitivity.

What makes saturated fat bad? Saturated fat causes more toxic breakdown products and mitochondrial dysfunction, and increases oxidative stress, free radicals and inflammation, establishing a vicious cycle of events in which saturated fat induces free radicals, causes dysfunction in the little power plants within our muscle cells (mitochondria), which then causes an increase in free radical production and an impairment of insulin signaling. I explain this in my video Lipotoxicity: How Saturated Fat Raises Blood Sugar.

Fat cells filled with saturated fat activate an inflammatory response to a far greater extent. This increased inflammation from saturated fat has been demonstrated to raise insulin resistance through free radical production. Saturated fat also has been shown to have a direct effect on skeletal muscle insulin resistance. Accumulation of saturated fat increases the amount of diacyl-glycerol in the muscles, which has been demonstrated to have a potent effect on muscle insulin resistance. You can take muscle biopsies from people and correlate the saturated fat buildup in their muscles with insulin resistance.

While monounsaturated fats are more likely to be detoxified or safely stored away, saturated fats create those toxic breakdown products like ceramide that causes lipotoxicity. Lipo- meaning fat, as in liposuction. This fat toxicity in our muscles is a well-known concept in the explanation of trigger for insulin resistance.

I've talked about the role saturated and trans fats contribute to the progression of other diseases, like autoimmune diseases, cancer and heart disease, but they can also cause insulin resistance, the underlying cause of prediabetes and type 2 diabetes. In the human diet, saturated fats are derived from animal sources while trans fats originate in meat and milk in addition to partially hydrogenated and refined vegetable oils.

That's why experimentally shifting people from animal fats to plant fats can improve insulin sensitivity. In a study done by Swedish researchers, insulin sensitivity was impaired on the diet with added butterfat, but not on the diet with added olive fat.

We know prolonged exposure of our muscles to high levels of fat leads to severe insulin resistance, with saturated fats demonstrated to be the worst, but they don't just lead to inhibition of insulin signaling, the activation of inflammatory pathways and the increase in free radicals, they also cause an alteration in gene expression. This can lead to a suppression of key mitochondrial enzymes like carnitine palmitoyltransferase, which finally solves the mystery of why those eating vegetarian have a 60 percent higher expression of that fat burning enzyme. They're eating less saturated fat.

So do those eating plant-based diets have less fat clogging their muscles and less insulin resistance too? There hasn't been any data available regarding the insulin sensitivity or inside muscle cell fat of those eating vegan or vegetarian... until now. Researchers at the Imperial College of London compared the insulin resistance and muscle fat of vegans versus omnivores. Those eating plant-based diets have the unfair advantage of being much slimmer, so they found omnivores who were as skinny as vegans to see if plant-based diets had a direct benefit, as opposed to indirectly pulling fat out of the muscles by helping people lose weight in general.

They found significantly less fat trapped in the muscle cells of vegans compared to omnivores at the same body weight, better insulin sensitivity, better blood sugar levels, better insulin levels and, excitingly, significantly improved beta-cell function (the cells in the pancreas that make the insulin). They conclude that eating plant-based is not only expected to be cardioprotective, helping prevent our #1 killer, heart disease, but that plant-based diets are beta-cell protective as well, helping also to prevent our seventh leading cause of death, diabetes.

This is the third of a three-part series, starting with What Causes Insulin Resistance? and The Spillover Effect Links Obesity to Diabetes.

Even if saturated fat weren't associated with heart disease, its effects on pancreatic function and insulin resistance in the muscles would be enough to warrant avoiding it. Despite popular press accounts, saturated fat intake remains the primary modifiable determinant of LDL cholesterol, the #1 risk factor for our #1 killer-heart disease. See The Saturated Fat Studies: Buttering Up the Public and The Saturated Fat Studies: Set Up to Fail.

How low should we shoot for in terms of saturated fat intake? As low as possible, according to the U.S. National Academies of Science Institute of Medicine: Trans Fat, Saturated Fat, and Cholesterol: Tolerable Upper Intake of Zero.

In health,

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:

Image Credit: Andrew Malone / Flickr

Original Link

Lipotoxicity: How Saturated Fat Raises Blood Sugar

NF-Nov24 Lipotoxicity How Saturated Fat Raises Blood Sugar copy.jpg

The reason those eating plant-based diets have less fat buildup in their muscle cells and less insulin resistance may be because saturated fats appear to impair blood sugar control the most.

The association between fat and insulin resistance is now widely accepted. Insulin resistance is due to so-called ectopic fat accumulation, the buildup of fat in places it's not supposed to be, like within our muscle cells. But not all fats affect the muscles the same. The type of fat, saturated vs. unsaturated, is critical. Saturated fats like palmitate, found mostly in meat, dairy and eggs, cause insulin resistance, but oleate, found mostly in nuts, olives and avocados may actually improve insulin sensitivity.

What makes saturated fat bad? Saturated fat causes more toxic breakdown products and mitochondrial dysfunction, and increases oxidative stress, free radicals and inflammation, establishing a vicious cycle of events in which saturated fat induces free radicals, causes dysfunction in the little power plants within our muscle cells (mitochondria), which then causes an increase in free radical production and an impairment of insulin signaling. I explain this in my video Lipotoxicity: How Saturated Fat Raises Blood Sugar.

Fat cells filled with saturated fat activate an inflammatory response to a far greater extent. This increased inflammation from saturated fat has been demonstrated to raise insulin resistance through free radical production. Saturated fat also has been shown to have a direct effect on skeletal muscle insulin resistance. Accumulation of saturated fat increases the amount of diacyl-glycerol in the muscles, which has been demonstrated to have a potent effect on muscle insulin resistance. You can take muscle biopsies from people and correlate the saturated fat buildup in their muscles with insulin resistance.

While monounsaturated fats are more likely to be detoxified or safely stored away, saturated fats create those toxic breakdown products like ceramide that causes lipotoxicity. Lipo- meaning fat, as in liposuction. This fat toxicity in our muscles is a well-known concept in the explanation of trigger for insulin resistance.

I've talked about the role saturated and trans fats contribute to the progression of other diseases, like autoimmune diseases, cancer and heart disease, but they can also cause insulin resistance, the underlying cause of prediabetes and type 2 diabetes. In the human diet, saturated fats are derived from animal sources while trans fats originate in meat and milk in addition to partially hydrogenated and refined vegetable oils.

That's why experimentally shifting people from animal fats to plant fats can improve insulin sensitivity. In a study done by Swedish researchers, insulin sensitivity was impaired on the diet with added butterfat, but not on the diet with added olive fat.

We know prolonged exposure of our muscles to high levels of fat leads to severe insulin resistance, with saturated fats demonstrated to be the worst, but they don't just lead to inhibition of insulin signaling, the activation of inflammatory pathways and the increase in free radicals, they also cause an alteration in gene expression. This can lead to a suppression of key mitochondrial enzymes like carnitine palmitoyltransferase, which finally solves the mystery of why those eating vegetarian have a 60 percent higher expression of that fat burning enzyme. They're eating less saturated fat.

So do those eating plant-based diets have less fat clogging their muscles and less insulin resistance too? There hasn't been any data available regarding the insulin sensitivity or inside muscle cell fat of those eating vegan or vegetarian... until now. Researchers at the Imperial College of London compared the insulin resistance and muscle fat of vegans versus omnivores. Those eating plant-based diets have the unfair advantage of being much slimmer, so they found omnivores who were as skinny as vegans to see if plant-based diets had a direct benefit, as opposed to indirectly pulling fat out of the muscles by helping people lose weight in general.

They found significantly less fat trapped in the muscle cells of vegans compared to omnivores at the same body weight, better insulin sensitivity, better blood sugar levels, better insulin levels and, excitingly, significantly improved beta-cell function (the cells in the pancreas that make the insulin). They conclude that eating plant-based is not only expected to be cardioprotective, helping prevent our #1 killer, heart disease, but that plant-based diets are beta-cell protective as well, helping also to prevent our seventh leading cause of death, diabetes.

This is the third of a three-part series, starting with What Causes Insulin Resistance? and The Spillover Effect Links Obesity to Diabetes.

Even if saturated fat weren't associated with heart disease, its effects on pancreatic function and insulin resistance in the muscles would be enough to warrant avoiding it. Despite popular press accounts, saturated fat intake remains the primary modifiable determinant of LDL cholesterol, the #1 risk factor for our #1 killer-heart disease. See The Saturated Fat Studies: Buttering Up the Public and The Saturated Fat Studies: Set Up to Fail.

How low should we shoot for in terms of saturated fat intake? As low as possible, according to the U.S. National Academies of Science Institute of Medicine: Trans Fat, Saturated Fat, and Cholesterol: Tolerable Upper Intake of Zero.

In health,

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:

Image Credit: Andrew Malone / Flickr

Original Link

Fat is the Cause of Type 2 Diabetes

NF-Nov17 What Causes Insulin Resistance copy.jpg

Studies dating back nearly a century noted a striking finding: If you take young, healthy people and split them up into two groups--half on a fat-rich diet and half on a carbohydrate-rich diet--we find that within just two days, glucose intolerance skyrockets in the fat group. The group that had been shoveling fat in ended up with twice the blood sugar. As the amount of fat in the diet goes up, so does one's blood sugar. Why would eating fat lead to higher blood sugar levels? It would take scientists nearly seven decades to unravel this mystery, but it would end up holding the key to our current understanding of the cause of type 2 diabetes.

The reason athletes carb-load before a race is to build up the fuel supply within their muscles. We break down the starch into glucose in our digestive tract, it circulates as blood glucose (blood sugar) and is taken up by our muscles to be stored and burnt for energy.

Blood sugar, though, is like a vampire. It needs an invitation to come into our cells. That invitation is insulin. Insulin is the key that unlocks the door that lets glucose in the blood enter muscle cells. When insulin attaches to the insulin receptor on the cell, it activates an enzyme, which activates another enzyme, which activates two more enzymes, which finally activates glucose transport (as diagrammed in my video What Causes Insulin Resistance?).

What if there was no insulin? Blood sugar would be stuck in the bloodstream banging on the door to our muscles, unable to get inside. With nowhere to go, sugar levels in the blood would rise and rise. That's what happens in type 1 diabetes: the cells in the pancreas that make insulin get destroyed, and without insulin, sugar in the blood can't get out of the blood into the muscles, and so blood sugar rises. But there's a second way we could end up with high blood sugar.

What if there's enough insulin, but the insulin doesn't work? The key is there, but something's gummed up the lock. This is insulin resistance. Our muscle cells become resistant to the effect of insulin. What's gumming up the locks on our muscle cells? What's preventing insulin from letting glucose in? Tiny droplets of fat inside our muscle cells, so-called intramyocellular lipid.

Fat in the bloodstream can build up inside the muscle cell, creating toxic fatty breakdown products and free radicals that block the insulin signaling process. No matter how much insulin we have in our blood, it's not able to sufficiently open the glucose gates and blood sugar levels build up in the blood. And this can happen within three hours. One hit of fat can start causing insulin resistance, inhibiting blood sugar uptake after just 160 minutes.

This mechanism by which fat induces insulin resistance wasn't known until fancy MRI techniques were developed to see what was happening inside people's muscles as fat was infused into their bloodstream. That's how we found that elevation of fat levels in the blood causes insulin resistance by inhibition of glucose transport into the muscles.

We can also do the opposite experiment. Lower the level of fat in people's blood and the insulin resistance comes right down. If we clear the fat out of the blood, we also clear the sugar out. That explains the finding that on the high fat, ketogenic diet, insulin doesn't work very well. Our bodies become insulin resistant. But as the amount of fat in our diet gets lower and lower, insulin works better and better--a clear demonstration that the sugar tolerance of even healthy individuals can be impaired by administering a low-carb, high-fat diet. We can decrease insulin resistance, however, by decreasing fat intake.

The effect is really dramatic--check out at least the end of my video What Causes Insulin Resistance? to see what happens as dietary fat intake drops.

The most concerning downside of low-carb diets, though, is heart health: Low Carb Diets and Coronary Blood Flow

This is the first of a 3-part series on the cause of type 2 diabetes, so as to better understand dietary interventions to prevent and treat the epidemic. In The Spillover Effect Links Obesity to Diabetes, I talk about how that fat can come either from our diet or excess fat stores, and then in Lipotoxicity: How Saturated Fat Raises Blood Sugar, I show how not all fats are equally to blame.

Here are some of my recent diabetes videos:

In health,

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:

Image Credit: [Gema Ibarra] © 123RF.com

Original Link

Fat is the Cause of Type 2 Diabetes

NF-Nov17 What Causes Insulin Resistance copy.jpg

Studies dating back nearly a century noted a striking finding: If you take young, healthy people and split them up into two groups--half on a fat-rich diet and half on a carbohydrate-rich diet--we find that within just two days, glucose intolerance skyrockets in the fat group. The group that had been shoveling fat in ended up with twice the blood sugar. As the amount of fat in the diet goes up, so does one's blood sugar. Why would eating fat lead to higher blood sugar levels? It would take scientists nearly seven decades to unravel this mystery, but it would end up holding the key to our current understanding of the cause of type 2 diabetes.

The reason athletes carb-load before a race is to build up the fuel supply within their muscles. We break down the starch into glucose in our digestive tract, it circulates as blood glucose (blood sugar) and is taken up by our muscles to be stored and burnt for energy.

Blood sugar, though, is like a vampire. It needs an invitation to come into our cells. That invitation is insulin. Insulin is the key that unlocks the door that lets glucose in the blood enter muscle cells. When insulin attaches to the insulin receptor on the cell, it activates an enzyme, which activates another enzyme, which activates two more enzymes, which finally activates glucose transport (as diagrammed in my video What Causes Insulin Resistance?).

What if there was no insulin? Blood sugar would be stuck in the bloodstream banging on the door to our muscles, unable to get inside. With nowhere to go, sugar levels in the blood would rise and rise. That's what happens in type 1 diabetes: the cells in the pancreas that make insulin get destroyed, and without insulin, sugar in the blood can't get out of the blood into the muscles, and so blood sugar rises. But there's a second way we could end up with high blood sugar.

What if there's enough insulin, but the insulin doesn't work? The key is there, but something's gummed up the lock. This is insulin resistance. Our muscle cells become resistant to the effect of insulin. What's gumming up the locks on our muscle cells? What's preventing insulin from letting glucose in? Tiny droplets of fat inside our muscle cells, so-called intramyocellular lipid.

Fat in the bloodstream can build up inside the muscle cell, creating toxic fatty breakdown products and free radicals that block the insulin signaling process. No matter how much insulin we have in our blood, it's not able to sufficiently open the glucose gates and blood sugar levels build up in the blood. And this can happen within three hours. One hit of fat can start causing insulin resistance, inhibiting blood sugar uptake after just 160 minutes.

This mechanism by which fat induces insulin resistance wasn't known until fancy MRI techniques were developed to see what was happening inside people's muscles as fat was infused into their bloodstream. That's how we found that elevation of fat levels in the blood causes insulin resistance by inhibition of glucose transport into the muscles.

We can also do the opposite experiment. Lower the level of fat in people's blood and the insulin resistance comes right down. If we clear the fat out of the blood, we also clear the sugar out. That explains the finding that on the high fat, ketogenic diet, insulin doesn't work very well. Our bodies become insulin resistant. But as the amount of fat in our diet gets lower and lower, insulin works better and better--a clear demonstration that the sugar tolerance of even healthy individuals can be impaired by administering a low-carb, high-fat diet. We can decrease insulin resistance, however, by decreasing fat intake.

The effect is really dramatic--check out at least the end of my video What Causes Insulin Resistance? to see what happens as dietary fat intake drops.

The most concerning downside of low-carb diets, though, is heart health: Low Carb Diets and Coronary Blood Flow

This is the first of a 3-part series on the cause of type 2 diabetes, so as to better understand dietary interventions to prevent and treat the epidemic. In The Spillover Effect Links Obesity to Diabetes, I talk about how that fat can come either from our diet or excess fat stores, and then in Lipotoxicity: How Saturated Fat Raises Blood Sugar, I show how not all fats are equally to blame.

Here are some of my recent diabetes videos:

In health,

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:

Image Credit: [Gema Ibarra] © 123RF.com

Original Link

Which are More Anti-Inflammatory: Sweet Cherries or Tart Cherries?

NF-Oct6 Anti-inflammatory life is a bowl full of cherries.jpg

Haggis, the national dish of Scotland, is a savory pudding of heart, liver, lungs, and oatmeal traditionally stuffed inside of a stomach. When that stomach goes into our own stomach, our digestive enzymes and stomach acid have no problem digesting it away. How do our bodies digests the stomach lining of a sheep on our plate without digesting our own stomach linings? It's meat and we're meat, so why don't we digest our own stomach every time we eat?

Partly because we have an enzyme called cyclooxygenase (COX) that protects the lining of our stomach. There are two types, COX-1 and COX-2. COX-1 is thought to be the primary protector of our stomach, whereas COX-2 is an enzyme responsible for pain and inflammation. In fact, anti-inflammatory drugs like ibuprofen and naproxen work by inhibiting the COX-2 enzyme. But these are non-selective drugs, so in addition to inhibiting COX-2 they also inhibit COX-1, which is trying to protect our stomach linings. Thus, although drugs like ibuprofen are great at relieving pain and inflammation, they kill thousands every year due to ulcerations through the stomach wall that result in life-threatening bleeding and perforation.

What are the risks on an individual level? On average, one in about 1,200 people who take this class of drugs for at least two months will die as a result. To put this into perspective, we can compare the death rate from anti-inflammatory drug side-effects to the risks associated with some well-known events. For example, it may be safer to go bungee jumping a few hundred times.

What we need is a selective COX-2 inhibitor, inhibiting the pain and inflammation of COX-2 without inhibiting the stomach protection of COX-1. We thought we got it with Vioxx, a blockbuster drug that brought in billions in profits before it started killing tens of thousands of peoples. Internal emails reveal how the drug manufacturer responded to the revelation that they were killing people: They drew up a list of doctors who were trying to warn people to "neutralize" them. If that didn't work, they tried to discredit them (You can see the emails in the video, Anti-inflammatory Life Is a Bowl of Cherries).

We're left then with two options: death from internal bleeding from one type of drug or death from side effects from another type of drug. If only there was some sort of natural COX-2 inhibitor. There is: cherries, which unlike ibuprofen suppress COX-2 more than COX-1.

In videos I did on insomnia and reducing muscle soreness (See Tart Cherries for Insomnia and Reducing Muscle Soreness with Berries), I talked about the benefits of sour cherries, the types of cherries used in baking. But sweet cherries, the kind you eat fresh, seem to be the MVP for COX-2 inhibition. Tart cherries had less of an effect. Regular red sweet cherries (Bing sweet cherries) were shown to have a greater anti-inflammatory activity than tart cherries. This makes sense since we think it may be the anthocyanin phytonutrients, and there are much more in sweet red cherries than in tart, and nearly none in yellow Rainer cherries.

Because fresh cherries have limited availability, what about other cherry products? In terms of anthocyanin phytonutrients, fresh is best, but frozen would appear to be the second-best choice.

Here are two ways I incorporate cherries into my diet:

Other studies in which anti-inflammatory drugs were compared natural dietary remedies include: Turmeric Curcumin and Osteoarthritis and Turmeric Curcumin and Rheumatoid Arthritis.

Anti-inflammatory activity in a test tube is one thing, but can cherries actually be used clinically to treat inflammatory diseases? See Gout Treatment with a Cherry on Top.

In health,
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, From Table to Able, and Food as Medicine.

Image Credit: Valdemar Fishmen / Flickr

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Why Do Heart Doctors Favor Surgery and Drugs Over Diet?

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When he was a surgeon at the Cleveland Clinic, Dr. Caldwell Esselstyn Jr. published a controversial paper in the American Journal of Cardiology, highlighted in my video, Fully Consensual Heart Disease Treatment, noting that heart bypass operations carry significant risks including the potential to cause further heart damage, stroke, and brain dysfunction. Angioplasty isn't much better, also carrying significant mortality and morbidity, and often doesn't work (in terms of decreasing the risk of subsequent heart attack or death). "So," he writes, "it seems we have an enormous paradox. The disease that is the leading killer of men and women in Western civilization is largely untreated." The benefits of bypass surgery and angioplasty "are at best temporary and erode over time, with most patients eventually succumbing to their disease." In cancer management, we call that palliative care, where we just kind of throw up our hands, throw in the towel, and give up actually trying to treat the disease.

Why does this juggernaut of invasive procedures persist? Well one reason he suggests is that performing surgical interventions has the potential for enormous financial reward. Conversely, lack of adequate return is considered one of the barriers to the practice of preventive cardiology. Diet and lifestyle interventions lose money for the physician.

Another barrier is that doctors don't think patients want it. Physician surveys show that doctors often don't even bring up diet and lifestyle options because they assume that patients would prefer to be on cholesterol-lowering drugs every day for the rest of their lives rather than change their eating habits. That may be true for some, but it's up to the patient, not the doctor, to decide.

According to the official AMA Code of Medical Ethics, physicians are supposed to disclose all relevant medical information to patients. "The patient's right of self-decision can be effectively exercised only if the patient possesses enough information to enable an informed choice. The physician's obligation is to present the medical facts accurately to the patient." For example, before starting someone at moderate risk on a cholesterol-lowering statin drug, a physician might ideally say something like:

"You should know that for folks in your situation, the number of individuals who must be treated with a statin to prevent one death from a cardiovascular event such as a heart attack or stroke is generally between 60 and 100, which means that if I treated 60 people in your situation, 1 would benefit and 59 would not. As these numbers show, it is important for you to know that most of the people who take a statin will not benefit from doing so and, moreover, that statins can have side effects, such as muscle pain, liver damage, and upset stomach, even in people who do not benefit from the medication. I am giving you this information so that you can weigh the risks and benefits of drugs versus diet and then make an informed decision."

Yet, how many physicians have these kinds of frank and open discussions with their patients? Non-disclosure of medical information by doctors--that kind of paternalism is supposed to be a thing of the past. Today's physicians are supposed to honor informed consent under all but a very specific set of conditions (such as the patient is in a coma or it's an emergency). However, too many physicians continue to treat their patients as if they were unconscious.

At the end of this long roundtable discussion on angioplasty and stents, the editor-in-chief of the American Journal of Cardiology reminded us of an important fact to place it all in context. Atherosclerosis is due to high cholesterol, which is due to poor dietary choices, so if we all existed on a plant-based diet, we would not have even needed this discussion.

The lack of nutrition training in medical school is another barrier. See, for example, my videos Doctors' Nutritional Ignorance and Doctors Know Less Than They Think About Nutrition.

Shockingly, mainstream medical associations actively oppose attempts to educate physicians about clinical nutrition. See my 4-part video series:

  1. Nutrition Education Mandate Introduced for Doctors
  2. Medical Associations Oppose Bill to Mandate Nutrition Training
  3. California Medical Association Tries to Kill Nutrition Bill
  4. Nutrition Bill Doctored in the California Senate

For more on why doctors don't make more dietary prescriptions, see my video The Tomato Effect, Lifestyle Medicine: Treating the Cause of Disease, and Convincing Doctors to Embrace Lifestyle Medicine.

Heart disease may be a choice. See Cavities and Coronaries: Our Choice and One in a Thousand: Ending the Heart Disease Epidemic.

-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: Leandro Ciuffo / Flickr

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How to Boost the Benefits of Exercise

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We all know exercise is beneficial to our health. Then why is it that ultramarathon runners may generate so many free radicals during a race that they can damage the DNA of a significant percentage of their cells? Researchers have looked at the exercise-induced increase in free radical production as a paradox: why would an apparently healthy act--exercise--lead to detrimental effects through damage to various molecules and tissues? This arises out of somewhat of a misunderstanding: exercise in and of itself is not necessarily the healthy act--it's the recovery after exercise that is so healthy, the whole "that-which-doesn't-kill-us-makes-us-stronger" notion. For example, exercise training has been shown to enhance antioxidant defenses by increasing the activities of our antioxidant enzymes. So, during the race ultra-marathoners may be taking hits to their DNA, but a week later they can experience great benefits, as shown in my video, Enhanced Athletic Recovery Without Undermining Adaptation.

In a recent study, researchers from Oregon State University looked at the level of DNA damage in athletes. Six days after a race, athletes didn't just go back to the baseline level of DNA damage, but had significantly less, presumably because they had revved up their antioxidant defenses. So, maybe exercise-induced oxidative damage is beneficial, similar to vaccination. By freaking out the body a little, we might induce a response that's favorable in the long run.

This concept, that low levels of a damaging entity can up-regulate protective mechanisms, is known as hormesis. For example, herbicides kill plants, but in tiny doses may actually boost plant growth, presumably by stressing the plant into rallying its resources to successfully fight back.

Wait a second, though. Could eating anti-inflammatory and anti-oxidant rich plant foods undermine this adaptation response? We know that berries may reduce inflammatory muscle damage (See Reducing Muscle Soreness with Berries), and greens may reduce free radical DNA damage (See Preventing Exercise Induced Oxidative Stress with Watercress). Dark chocolate and tomato juice appear to have similar effects. How it works is that flavonoid phytonutrients in fruits, vegetables, and beans seem to inhibit the activity of xanthine oxidase, considered the main contributor of free radicals during exercise. And the carbs in plant foods may also decrease stress hormone levels.

So in 1999, a theoretical concern was raised. Maybe all that free radical stress from exercise is a good thing, and increased consumption of some antioxidant nutrients might interfere with these necessary adaptive processes. If we decrease free radical tissue damage, maybe we won't get that increase in activity of those antioxidant enzymes.

A group of researchers who performed a study on tart cherry juice and recovery following a marathon responded to this antioxidant concern by suggesting that, although it is likely that muscle damage, inflammation, and oxidative stress are important factors in the adaptation process, minimizing these factors may improve recovery so we can train more and perform better. So, there are theories on both sides, but what happens when we actually put it to the test?

While antioxidant or anti-inflammatory supplements may prevent these adaptive events, researchers found that blackcurrant extract - although packed with antioxidant and anti-inflammatory properties - actually boosted the health benefits of regular exercise.

If we take antioxidant pills--vitamin C and vitamin E supplements-- we can also reduce the stress levels induced by exercise, but in doing so we block that boost in antioxidant enzyme activity caused by exercise. Now maybe we don't need that boost if we don't have as much damage, but vitamin C supplements seem to impair physical performance in the first place. With plant foods, though, we appear to get the best of both worlds.

For example, lemon verbena, an antioxidant-rich herbal tea, protects against oxidative damage and decreases the signs of muscular damage and inflammation, without blocking the cellular adaptation to exercise. In a recent study, researchers showed that lemon verbena does not affect the increase of the antioxidant enzyme response promoted by exercise. On the contrary: antioxidant enzyme activity was even higher in the lemon verbena group. In my video, Enhanced Athletic Recovery Without Undermining Adaptation, you can see the level of antioxidant enzyme activity before and after 21 days of intense running exercises in the control group. With all that free radical damage, the body started cranking up its antioxidant defenses. But give a dark green leafy tea, and not only do we put a kabosh on the damage due to all the phytonutrients and antioxidants, but we still get the boost in defenses--in fact, in this case, the boost was even greater.

Find out more on enhancing athletic recovery in this three-part video series:

1. Reducing Muscle Fatigue with Citrus
2. Reducing Muscle Soreness with Berries
3. Preventing Exercise-Induced Oxidative Stress With Watercress

Then there's my 15-video series on using nitrate-rich vegetables to boost athletic performance starting with Doping With Beet Juice and ending with So Should We Drink Beet Juice or Not?

-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.

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Chronic Headaches and Pork Parasites

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Neurocysticercosis is the sciencey name for an infection of the human central nervous system by pork tapeworm larvae. The invasion of baby pork tapeworms in the brain "has become an increasingly important emerging infection in the United States," and is the #1 cause of epilepsy in the world. It is the most common parasitic disease of the human brain and used to be found throughout only the developing world (with the exception of Muslim countries, since less pork is consumed there). That all changed about 30 years ago, and now it's increasingly found throughout North America.

Besides seizures, the pork parasites may actually trigger brain tumors or cause an aneurism or psychiatric manifestation like depression. It can also result in dementia, but with deworming drugs this is often reversible. Only rarely do surgeons have to surgically remove the larvae.

I've talked about pork tapeworms before (see my videos Pork Tapeworms on the Brain, Avoiding Epilepsy Through Diet, and Not So Delusional Parasitosis). What's new is that we now know that they may present as chronic headaches--either migraines or so-called "tension-headaches"--even when the worms in our head are dead. What researchers think is happening is that as our body tries to chip away at the worms' calcified bodies, bits of them may be released into the rest of our brain causing inflammation that could be contributing to headaches.

This condition is rare even in endemic areas, but we can avoid getting infested with an adult tapeworm in the first place by cooking pork thoroughly. It's found in some parts of pig carcasses more than others (see the meat chart here), and the worms can be frozen to death no matter how infested the muscles are by storing pork (cut up into small pieces) for a month at subzero temperatures. Then to ensure the larvae are dead the meat is recommended to be cooked for more than two hours. That's one well-done pork chop!

The New England Journal of Medicine recently featured a case of some guy who must have had thousands of pork tapeworm larvae wriggling through his muscles. In my video, Chronic Headaches and Pork Tapeworms, you can see an x-ray, showing the thousands of little white streaks in this man's body. Each white streak is a baby tapeworm. That's why you can get infected by pork, it gets in the muscles. So cannibals might want to cook for two hours too.

Not all parasites are associated with meat, though. An anxious but healthy 32-year-old male physician presented to the family medicine clinic with a sample of suspected parasites from his stools, which had been retrieved from the toilet that same day. They looked to be about an inch long. He had previously traveled to India, had Chinese food the night before--who knows what he had. Maybe it was hookworms? The sample was sent to the microbiology laboratory for analysis. Later that day, the microbiology physician called to report positive identification of Vigna radiata (previously known as Phaseolus aureus) in the stool sample. Or in common parlance, a bean sprout. They were bean sprouts!

"The patient was called and gently but firmly informed of the diagnosis. Given the nature of the identified specimen, the information was presented in a non-judgmental, respectful manner so as not to offend the sensibilities or sensitivities of the patient."

Their parting advice to fellow physicians in cases of this nature was as follows: "as comical as the findings might seem--try not to laugh!"

Other parasites in meat include toxoplasma (Brain Parasites in Meat), sarcosystis (USDA Parasite Game), and Anisakis (Allergenic Fish Worms). There can even be critters in some dairy products (Cheese Mites and Maggots). Eating Outside Our Kingdom describes a brain malady caused not by meat parasites, but by meat proteins themselves.

One of the nice things about eating plant-based is that plant parasites, like aphids, don't affect people. When is the last time you heard of someone coming down with a bad case of Dutch elm disease?

If you haven't yet, you can subscribe to my videos for free by clicking here.

-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: ML Cohen / Flickr

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