Monday, August 17, 2020

Why vegetarians have less heart disease.


We know that those with diets higher in plant foods (and lower in animal foods) have a decreased risk of heart attack and stroke (as well as less diabetes and even cancer).

The favorite culprit is the high fat and cholesterol content of animal meats. A second is high-temperature cooking (pan-frying, grilling) producing cancer causing and other harmful intermediary compounds.

Although both may be contributing factors, more and more evidence is pointing to two proteins found in all red meat - carnitine and the cell sugar-protein molecule Neu5Ac - as the root cause of severe blood vessel disease.

Carnitine is a muscle protein. After digestion, carnitine absorbed and processed in the liver into trimethylamine (TMA) which is in turn modified by colon bacteria (our microbiome) into trimethyl n-oxide (TMAO).

In lab experiments, TMAO is directly toxic to blood vessel lining cells. The injured cells absorb fats from the circulation which results in the formation of blood vessel plaques, and in the presence of high blood fat and cholesterol levels, the process is accelerated.

A clinical parallel has been identified in studies on patients seen in hospital ERs for chest discomfort. Those with the highest blood levels of TMAO (compared to the lowest) are  six times as likely to die within the following month and twice as likely to die within seven years.

Vegetarians as a group have the lowest average blood levels of TMAO. Interestingly, when given a single dose of carnitine (a piece of steak) their blood TMAO levels barely budge. The reason? A person's microbiome responds to their diet. Expose the colon bacteria to more of a specific food and those that thrive on it multiply. Being exposed to only small amounts of carnitine in a no-meat diet, there are very few carnitine metabolizing bacteria available to process that occasional steak. This suggests that an occasional meat containing meal should be less harmful to your blood vessels than when it is part of your daily diet.

The second meat protein is Neu5Gc, a cell surface protein found on all non human mammalian cells (but not chicken or fish). Eons ago a genetic mutation in humans led to its modification to a similar molecule (Neu5Ac). As this new protein provided some protection against malaria, it became the dominant form.

Our immune system recognizes invading germs by their cell surface proteins. When it detects proteins that are different from our own, antibodies to kill the invading germs are produced.

With this change in our cell sugar-protein, the immune system now sees all non human mammal meat as “different”, the immune system revs up, and antibodies are formed. The result is that those who regularly eat beef (a mammal meat) have blood markers reflecting a state of chronic inflammation.

A side effect of the overactive immune system is collateral damage to cells throughout the body. In the blood vessels this means more atherosclerosis with an increased risk of heart attacks and strokes, and in other cells the damage increases the risk of cancer.

Supportive evidence once again comes from the laboratory where mice, genetically altered with the human gene mutation and placed on a meat diet have twice the heart attack risk of genetically unmodified mice on a similar diet.

These two harmful effects of a mammal meat diet are moderated to a degree by small molecules produced from the metabolism of fiber by our microbiome. But with most red meat containing diets being lower in fruits,vegetables and whole grains, this protection is weakened. The effect is observed in those on a strict paleo diet (high red meat and no whole grain) who have much higher blood TMAO levels than those who eat even a small amount of whole grain.

What does this body of work suggest as far as healthy diet changes?

First, cut red meat intake and decrease exposure to the toxic effects of TMAO. In one large study, there was a 10% (one in ten) decrease in heart disease deaths in those who cut their red meat intake to an average of half a serving per day! Alternatives to be considered are poultry, fish, nuts, legumes, low-fat dairy, and whole grains.

Second is to take advantage of the protective effects of fiber. The benefits of additional servings of fruits and vegetables have been shown to increase up to 10 servings per day.

Finally, it is never too late to make a change. Health professionals who began eating more whole grains, fruits, vegetables, and fish were able to significantly lower their risk for death in as few as 8 years.

References




















Egg and cancer risk via TMAO

Nice summary of non heart disease risks of TMAO https://nutritionfacts.org/video/can-vegan-fecal-transplants-lower-tmao-levels/ 
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Sunday, January 19, 2020

Fat metabolism and the ketogenic diet


Fats provide 20 to 40% of the calories in an average daily American diet.

More than 95% of dietary fat is in the form of triglycerides which are a combination of three fatty acid (FA) molecules and a single glycerol molecule. The other 5% is cholesterol and phospholipids. Triglycerides are an important energy source while the cholesterol and phospholipids are important as building blocks for cell growth.

In the small intestine, triglycerides are cleaved into their component molecules – glycerol and fatty acids. The fatty acid molecules are then transported through the intestinal lining cells into the blood. As they circulate, they diffuse through cell membranes throughout the body where they are either directly metabolized as an energy source or reconstituted into triglycerides for storage for future use.

The bulk of the body's 50,000 – 60,000 stored fat calories are in fat cells (lipocytes) with 2,000-3,000 additional calories stored in liver and muscle cells.

Both fatty acids and glycogen (the storage form of carbohydrates) are metabolized into the same energy containing compound, Adenosine Triphosphate (ATP), to provide energy for the body's cells.

Decades of research suggested that a diet low in fat, with the bulk of daily calories from carbohydrates, was the healthiest diet. But in the past few years that recommendation has come into question.

Instead it's been found that replacing carbohydrate calories with fat calories may be the healthier approach, actually increasing HDL (good cholesterol) which suggests less long term cardiovascular disease.

 And dieting with 33% of daily calories from fat was actually a more effective long term weight loss strategy than a diet with fats limited to only 20% of daily calories.

If that's the case, why all the interest in a ketogenic diet?

The basis of both the Atkins low carbohydrate and the more severely carbohydrate restricted ketogenic diet was speculation that the combination of carbohydrate restriction, combined with calorie restriction, would force the body to turn to fatty acid metabolism for energy and in turn increase the rate of fat (weight) loss.

When there are inadequate carbohydrate calories available, we know cells use fat to power cells with the metabolic end product being ketones. This occurs overnight, when fasting, and in diabetics where carbohydrates cannot get into the cells. The cells turn to fat for fuel, and the patient becomes ketotic with an acetone (a ketone) smell on their breath.

Although logic supports the ketogenic argument, the ultimate outcome is not what we would predict.

Initially, a ketogenic diet gives dramatic results. On a standard calorie restricted diet, a study group lost about a pound a week. Switched to a ketogenic diet this increased to 3 ½ pounds in the first week.

But further investigation of their body composition found that the rate of fat loss had decreased by 50% with the bulk of the extra weight loss from water weight. It appeared that the with carbohydrate restriction, the body began cannibalizing its own protein for energy instead of using fat. The group lost less fat and more protein (and water).

In a real life scenario, a group of CrossFit trainees switched to a ketogenic diet based on the assumption that a switch to a fat based metabolism would help their endurance performance. They found their leg muscles shrank by 8%. Not the trade off they were expecting.

The moral to the story? Fats, protein, and carbohydrates all have a place in a healthy diet. Your body evolved to use carbohydrates to fuel muscle activity. While excess carbohydrates beyond those needed for daily activities are converted into fat, too few are also a problem as the body scavenges needed energy from the protein of its own cells.

References:

http://www.cptips.com/fat.htm

https://journals.sagepub.com/doi/pdf/10.1177/0310057X1804600506  Ketosis with fasting

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5309297/   Ketones and exercise, with good set of references.

https://onlinelibrary.wiley.com/doi/full/10.1002/(SICI)1520-7560(199911/12)15:6%3C412::AID-DMRR72%3E3.0.CO;2-8?sid=nlm%3Apubmed  Ketone metabolism.
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Thursday, December 19, 2019

Time restricted eating.


Counting calories for weight management is not only tedious but ultimately ineffective. Clinical studies confirm that most dieters increasingly skip the counting, stray from their diets, and in the long run regain lost weight. 
Intermittent fasting (or time restricted eating) offers an effective alternative to calorie counting.
By limiting pancreas stimulation, it is also beneficial for patients with metabolic syndrome, pre-diabetes, and diabetes,  all of which are linked by altered insulin metabolism.
We all fast when we are asleep, and then eat from 7 AM to 6 PM with a snack later in the evening. Ergo most of us have an eating interval of 12 or 13 hours alternating with a fasting interval of 11 or 12 hours.
Intermittent fasting as currently used in the literature (time restricted eating is technically more correct) refers to extending the length of our normal night time fast in conjunction with restricting our daytime eating hours. One of the most popular versions of intermittent fasting is called the 16:8 plan. You eat during an eight-hour window, say, from noon to 8 p.m., and then fast for the other 16. 
There is a solid rationale for extending a daily fast rather than alternating 4 or 5 days of a normal eating with 2 or 3 complete fasting days per week.  The daily schedule synchronizes your calorie intake with the body’s normal 24 hour circadian cycle, the master clock controlling multiple metabolic digestive processes. Vary the timing of eating from day to day and these processes get out of sync. Likewise the eating window should start at about the same time every day.

The distribution of daily calories across the eating interval is important. During physical activity, muscle cells actively remove glucose from the blood (to fuel contraction) and blunt a rise in blood glucose. Eating early in the day means less insulin is released to divert dietary calories into liver fat or fat cells. Thus it makes sense to distribute total daily calories 25-50-25 percent rather than, let’s say, 25-25-50 which leaves the bulk of any blood sugar rise occurring while you are more sedentary at the end of the day.

In this recent study on intermittent fasting nineteen individuals shortened their normal daily eating interval of 15 hours to 10 hours without limiting their calories,  the kinds of food that they ate, or how much they exercised.
The results?
  • Individuals ate an average 200 fewer calories per day (without trying) and lost an average of 7 pounds over the following 3 months.
  • They lost three percent of their body fat and reduced their belly fat by three percent
  • They lowered their high blood pressure, bad LDL cholesterol, fasting blood sugar, triglycerides, and HBA1c (a measure of poor blood sugar control).
How does limiting pancreas stimulation and minimizing blood insulin levels lead to these benefits?
When blood sugar levels rise, the pancreas responds by releasing insulin and glucose (sugar) is moved from the bloodstream in to liver and fat cells for storage.The fat cells grow larger and we gain weight. The liver also converts excess sugar calories into fat. Liver fat in turn blunts the effectiveness of insulin, the cause of metabolic syndrome, pre-diabetes, and diabetes.
Time restricted eating has become a popular weight loss strategy as many people find it easier to follow than traditional calorie restriction diets. And best of all, after the study was completed, nearly 70 percent of the participants reported that they were sticking with the diet on their own. 
Best of all, time-restricted eating is the healthiest way to eat, whether or not you are working on weight management.


https://www.cell.com/cell-metabolism/fulltext/S1550-4131(19)30611-4

 https://nutritionfacts.org/video/the-benefits-of-early-time-restricted-eating/


https://nutritionfacts.org/video/eat-more-calories-in-the-morning-to-lose-weight/
https://www.medscape.com/viewarticle/923557_1 (may need password)

https://www.drmirkin.com/nutrition/long-total-fasts-may-be-harmful.html

---
Added after publication. Why time restricted eating works.
https://www.drmirkin.com/nutrition/why-intermittent-fasting-works.html 
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Sunday, November 24, 2019

Hijacking our autonomy.


The debate on the extent to which our behavior is the result of our nature (our inheritance) versus nurture (our life experiences) is one of the oldest topics in psychology. Think of nature as the genetically based pre-wiring of our brain and nurture as the influence of post conception external factors such as our culture and what we learn.



Over the last half century there has been an increased appreciation of the importance of genetics in decision making. Fifty years ago it was taught that how we were raised was by far and away the most significant factor shaping beliefs and how we lead our lives.



Today we find the pendulum has shifted and it is our genes (DNA) that are thought to have the greater impact - perhaps as much as 80%.



But genetics and past experiences are just modifiers and a final  decision is still our choice and not predestined…..maybe. Additional modifiers have been identified and suggest our free will may not be quite as free as we’d like to think.



How we react to our world is the result of the complex interaction of many small molecules (chemical neurotransmitters) at the connection of the brain nerve cells. And we now have many examples of how this interaction can be biased by various biologic agents.



An good example is a tropical ant infected with a species specific fungus. The fungal cells produce a chemical (a neurotransmitter) that leads to very un-ant like behavior. Just before dying, the ant leaves its nest and climbs a nearby plant.  It then bites down on a leaf and its jaws lock as it dies. The fungus then completes its own life cycle with the resulting spores now more easily spread by the wind.



Toxoplasma, a parasite that normally infects cats, presents a similar possibility in humans. Humans are not the usual intermediary host (which is a mouse or rat in the wild) but can be inadvertently infected. Blood work indicates as many as 1 in 4 adults have been infected during their life but a healthy immune system keeps the parasite in check.



In the mouse, the parasite hijacks the nervous system in a way that increases the odds of an infected mouse being eaten by its appropriate host, the cat. The rodent’s inborn avoidance of cat odor is dampened and its response time and coordination are slowed. So when a cat finally does pounces, the parasite has shifted the odds away from the mouse escaping.



Studies suggest parallel neurologic changes in infected humans. Data show an above average percentage of prior toxoplasmosis infections in several diseases associated with disordered thinking (schizophrenia, bipolar), as well as more frequent traffic and work site accidents which raises the possibility of slowing reflexes and coordination as well.



The toxoplasmosis parasite likewise uses neurotransmitters manipulation. They have a unique enzyme that makes dopamine (a neurotransmitter) to release into surrounding brain tissue. 



The microbiome is another example of a biologic agents that may influence our thinking. These bacteria (in our large intestine) produce a number of small molecules, among them the same chemicals (dopamine, serotonin and gamma-aminobutyric acid) used by the brain’s neurons to communicate with each other and to regulate mood.



Just as with toxoplasmosis, investigations have uncovered specific variations in the microbiome of patients with a wide range of neurologic and psychiatric conditions, including depression, autism, schizophrenia, and bipolar disorder. Whether these changes are the cause of these conditions and not a result is still being sorted out.



And the list goes on. Including chemical plasticizers (in our water bottles) with endocrine like effects as well as a similar potential in the over 2000 new chemical agents being added to the environment annually.



In the end we are still in charge of our decisions, but these examples suggests we should not take that freedom for granted.


References:
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Thursday, October 10, 2019

Using fiber to manage our weight


Statistics from early 2019 show the US obesity rate approaching 40 percent after holding steady around 35 percent a decade earlier. These numbers are even more startling when you consider it was only 20 years ago that no state had an adult obesity rate greater than 15 percent.



What’s behind this trend? Most authorities point to diet rather than lifestyle. We just eat too much, more calories than we use.  And the excess are stored for the future. Our weight sneaks up.



How does our diet differ from past generations? The most likely explanation is a shift in the ratio of plant to animal protein.



Man has been an omnivore (eating both animals and plants) for at least a million years. A unique bone disease associated with vitamin B12 deficiency (a vitamin found only in animal meat and dairy products) is proof that man has always needed some animal protein in his diet.



But analysis of fossilized feces (paleopoop) suggests that meat was a rare treat in a diet containing more than 100 grams of plant fiber a day.



With plants the primary source of nutrition, it has been speculated that it was the fiber in our ancestor’s diet that sent the signal we had eaten enough. Dietary fiber is metabolized in the colon into short chain fatty acids (SCFA). These SCFAs in turn can affect multiple metabolic pathways so it is not unreasonable to conclude they might provide the satiety signal. Eat less fiber, fewer SCFAs are produced, and we remain on the hunt for more food. So it may be the absence of adequate fiber in our diet that is the trigger to keep pouring in the calories.



Now let’s jump ahead a million years to one of the biggest changes in man’s diet over the last 50 years - the explosive increase in processed foods.



Strictly speaking, a processed food is any grocery item that has been modified from its original form.  But processing covers much more than just mechanical alteration and can include the removal of fiber as well as  fortification with additional fats as well as sugar and salt. 



Why pick on processed foods?



Twenty people, in a month long controlled study, ate an unlimited diet of highly processed foods for two weeks and then switched to unprocessed or minimally processed foods for a second two weeks. On a processed diet they ate an average of 500 more calories per day and gained an average of two pounds over the two weeks. Then on an unprocessed diet lost an average of two pounds.



There are several possible explanations.



On processed foods,  subjects ate nearly 50 calories per minute but only 32 calories per minute on unprocessed foods. Eating processed foods means you can eat more calories before your stomach signals your brain you are full. It takes far more time to chew up unprocessed foods before you swallow them, and eating more slowly usually means you eat less.



Another possibility is the form and size of the food particles. Carbohydrates, fats and proteins all must be reduced to simpler single sugars, amino acids, and fatty acids before they can be absorbed into the blood stream.



Processing reduces the size of food particles and makes further digestion that much easier.  This in turn increases the calories you absorb from that food. Grinding whole grains into flour or cooking starchy vegetables increases the number of calories you absorb from those foods.



Cooking itself modifies foods and increases absorption. Boiling, baking or frying modifies starches, markedly increasing the calories you will absorb from root vegetables such as potatoes, turnips, cassava, yams, and rutabagas.



One has to consider energy density. Even before digestion the added sugar and oils increase the calories per ounce in processed food. The same portion size contains more calories.



And finally there is the fiber argument. Less fiber for the microbiome and fewer SCFAs for the satiety feedback loop. Not to mention that processed foods contain emulsifiers as a way to prolong shelf life and keep ingredients from separating.  In mice emulsifiers disrupt intestinal bacteria (the microbiome) resulting in weight gain. If these same changes occur in the human colon, emulsifiers may be another piece of the weight gain explanation as they mean any fiber reaching the colon could be less effective in SCFA production.



What does this all mean for weight management? A few simple changes in your diet, a few less calories per day,  can pay big rewards over time.



Eat fewer processed foods. Change your route through the store. Ultra - processed foods lurk in the center aisles.  Walk the perimeter with its fresh fruits and vegetables first and go down the aisles only when you have a specific item in mind.



Add more fresh fruits and vegetables to your diet. Especially fruits and vegetables that are not cooked, ground or softened. They are great as a snack alternative.



And eat more whole grains, beans, seeds and nuts that have not been ground into flour. This includes fewer foods made from flour such as bakery products and pastas.



It will take some planning, but using what you know about fiber provides an opportunity to quit counting calories.

References:



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Friday, September 6, 2019

What's new in colon cancer?


Colorectal cancer is the second leading cause of cancer death in the United States and the third most common cause of cancer death in the world. Your lifetime risk of developing colorectal cancer is a bit less than 1 in 20.


But there is a light on the horizon. Since 2000, the diagnosis rate for those 50 and older has dropped by a third with recent work on screening and prevention showing how we can improve the numbers even further.


Colon cancer starts in the lining cells of the large intestine in a “two hit” process.


The first step, theorized to be an exposure to an environmental toxin or infectious agent in a genetically predisposed individual, initiates the rapid growth of a single cell which then, over time, grows into a benign polyp.


A second change then occurs in one of these rapidly growing polyp cells results in the first cell of a colon cancer. If this polyp is removed at this early stage, the small cancer is cured.


Left in place, however, the cancer slowly increases in size until at some point it grows through the wall of the colon. It has been estimated that the time from benign polyp to colon wall cancer is in the neighborhood of 10 years.


This physiology is the basis for screening colonoscopy. Identify and remove polyps and you will prevent, and in some cases, cure colon cancer.


The effectiveness of colonoscopy screening is the likely explanation of the drop in the rate of colon cancer diagnosis over the last 20 years. It has been estimated that over 60% of people over 50 years old have been screened.


The first of the new developments is an easier but equally effective screening test. Advances in immunologic testing allows low risk individuals to collect a small stool sample for testing. Individuals with low risk have no personal or family history of colon cancer or polyps. The stool is then tested for remnants of abnormal proteins shed by polyps. The colonoscopy is reserved to evaluate for and remove polyps only in those who are stool test positive.


This annual fecal immunochemical test (FIT) gives physicians an additional tool to take advantage of that 10 year screening window. More screening equals earlier removal (and cure) of more small colon cancers. The FIT is inexpensive, seemingly as effective as colonoscopy screenings, and more readily available to patients.


The next advance suggests we may be getting closer to the idea of preventing colon cancer rather than just finding it in its early, curable stages. It looks like colon cancer might be an infectious disease.


Thirty years ago, we found that stomach ulcers are often the result of a bacterial infection (H. Pylori) of the digestive tract, rather than the result of acid irritation alone. We now have suggestive evidence that a certain bacteria may be associated with those cell changes that lead to colon polyps and colon cancer.


High concentrations of a family of bacteria (Fusobacterium) were found in colon cancer tissue removed from more than 1000 people at surgery. Even more interesting was finding the same bacteria in an occasional colon metastases (cancer that had spread), implying an even stronger linkage. The benefits of targeting and eliminating this specific colon bacteria (with antibiotics or diet) is being investigated.


And finally, while studying the role of colon bacteria as a cause of colon cancer, there were clues as to how our diet may play a role in the initiation or inhibition of cancerous cell growth. That means making changes in our diet might decrease our personal risk of developing colon cancer.


It’s old news that vegetarians have less colon cancer, 20 - 30 percent less than non-vegetarians. But why?


One possibility could be the elimination of a cancer cell stimulant. Studies of groups on high versus low meat diets revealed a three fold variation in the concentration of nitrosamines, a potentially cancer causing compound, in their stool.


Another might be the addition of an actual inhibitor of cancer growth. The microbiome produces short-chain fatty acids as it metabolizes dietary fiber. Laboratory experiments exposing colon cancer cells to one of them, butyrate, slows and can even stop cancer cell growth. Take away the butyrate and the cells resume growing.


More fruits and vegetables, less red meat, and it appears you can impact your colon cancer risk.


Even after colon cancer’s development, diet changes impact a patient’s future course. In a study of 1,000 people already diagnosed with colon cancer spread beyond the colon, those who modified their lifestyle to a healthier diet with added exercise decreased their risk of dying over the next seven years. The risk was decreased by 42 percent compared to those who did not change their diet.



Better screening, prevention with simple diet changes, and the chance that we might eliminate one reason for that first cancer cell are three reasons I’m optimistic that the trend line for colon cancer diagnosis (and deaths) will continue on a downward trend.

References:











Aspirin may decrease CRC by its effect on the microbiome. https://www.medscape.com/viewarticle/937141

Egg and colon cancer risk via TMAO

Less meat/alcohol and more dairy = less colon cancer

https://www.medscape.com/viewarticle/958688 
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Thursday, August 1, 2019

Coffee - a health risk?


Coffee is one of the most commonly consumed beverages worldwide. Two thirds of Americans drink at least one cup of coffee a day, with the average consumption at 3.1 cups of coffee per day. In the US that’s 400 million cups of coffee a day or 146 billion cups of coffee per year.



Although that is a lot of beans, we are not even close to being a leader in per capita consumption. Finland comes in first at 12 kg of coffee per person per year with the other scandinavian countries - Sweden, Norway, and Denmark - close behind. The US places a distant 25th at 4.2 kg per person per year.



Which brings up the question as to whether all this coffee is affecting our health.  Is Starbucks vying with fast food as a leading contributor to our country’s declining longevity?



Roasted coffee is a complex mixture of more than 1000 bioactive compounds including caffeine and a number of antioxidants.  For those who drink coffee, it provides more of their daily dietary antioxidants than tea, fruit, and vegetables.



A 2017 analysis of over 200 individual studies documented a health benefit for coffee drinkers and the more cups a day, the greater the reduction in all cause mortality. There was  a decrease in heart disease and cancer as well as a number of neurologic conditions. Decaffeinated coffee was as beneficial as caffeinated coffee in its health impact. 



The longevity benefit (approximately 3% per cup) was greatest for the first four cups but even a fifth and sixth cup added an additional boost. The final numbers are impressive. A 17% reduction in all cause mortality, an almost 20% reduction in cardiovascular disease, and a similar reduction in cancer.



The liver fared even better with a 29% lower risk of non-alcoholic fatty liver disease and a 39% lower risk for liver cirrhosis (scarring). 



As did the brain. Coffee drinkers have a lower rate of developing Parkinson’s disease, a decreased risk of depression, and an amazing 25% decrease in the incidence of Alzheimer’s disease. Interestingly, a single randomized study focused on Parkinsonism, there was an improvement in movement symptoms after just three weeks of two cups of coffee a day.



Even the current diabetic epidemic was impacted positively with a 25% risk reduction.



Athletes have long taken advantage of the improvement in athletic performance with just a single cup of coffee - runners randomized to drink coffee shaved about six seconds per mile off their times while weightlifters could squat more weight. 



What about risks? 



There is a marginal increase in complaints of esophageal reflux (heartburn and indigestion).



Fracture risk is increased in women (only) -  one percent with one cup a day rising to 14% at higher daily intakes.



Interestingly there was one cancer that is statistically more common in regular coffee drinkers - ovarian cancer. The reason is not clear and this may be a statistical blip.



Coffee has a cholesterol raising effect which parallels increasing intake of unfiltered coffee. It is speculated that an oily substance in the bean, removed with a paper filter, is the culprit.  The implications of this observation are uncertain as increasing coffee consumption is not associated with more adverse cardiovascular outcomes, including myocardial infarction.



Coffee should be avoided in pregnancy based on a well documented association with low birth weight, preterm birth, and miscarriage.  Most obstetricians suggest pregnant women limit their caffeine intake to 200 milligrams (one small cup of coffee) a day.



Although most of us have heard about the risk of extra heart beats (palpitations and atrial fibrillation) from too much coffee, data shows the opposite to be true.  Caffeine does not increase the risk of atrial fibrillation. And low doses of caffeine, defined in the study as less than five cups of coffee a day, may even have a protective effect.
Finally, let’s not forget those with insomnia who are especially sensitive to the effects of caffeine.



Where does this leave us? My take aways:



1) If you are pregnant, cut back your coffee.



2) If you have a history of osteoporosis with its increased risk of fractures, cut back on your coffee.



3) Otherwise drink as many cups a day as you’d like, the more the better. We’re not yet at the point of prescribing coffee for specific diseases, but like aspirin it is a readily available, over the counter product, with surprising health benefits.
References:






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