I can honestly say that I have never been a fan of calcium supplementation. Or at least maybe not for the last decade or so.
It has truly been that long since the medical research began to change its opinion on using calcium supplements to strengthen bones. This is not to say that I don’t recommend calcium supplements, but it is a pretty rare situation and only when someone has been diagnosed (in our office or elsewhere) with severe osteoporosis. It has been a long, long time since I recommended calcium for anyone just to “build strong bones.”
Before we go any further, I do need to clarify something about calcium supplements for bone health. Tums are NOT a calcium supplement. It is a toxic product containing aluminum and artificial colors and should never, ever have been recommended to support bone health.
Any calcium supplement used for bone health should be a bone support formula, containing not only calcium, but other bone-supporting components like magnesium, boron and zinc. And the best form of calcium is NOT calcium carbonate. Higher quality forms like citrate are the preferred forms–especially when it matters.
Another thing that you may not realize is that your body is very selective as to how much calcium it will absorb at any given time. This is because calcium levels are very tightly regulated in the bloodstream. Too much or too little calcium can be fatal. As in rigor mortis, the ultimate calcium deficiency in the bloodstream. To keep this level constant, the gut keeps a very tight grip on how much calcium is absorbed at any given time. If you decide to down an entire bottle of calcium supplements at a single time, the gut will actually push back, resulting in even lower amounts of calcium being absorbed.
This is why, when you are taking calcium supplements, you should take them spread out throughout the day as much as possible.
But none of this really matters because of one important fact.
Vitamin D plays a very large role in regulating the amount of calcium you gut will absorb (it’s role is much bigger, but for the purposes of this particular line of discussion, this will suffice). With low levels of vitamin D (an all-too common problem in todays’ sun-fearing society) more calcium may not be enough to get the job done. On the flip side, having enough vitamin D flowing through your blood will make taking a calcium supplement pointless on top of a good quality diet.
Unfortunately, for years, doctors were telling their patients to take calcium supplements (frequently in the form of Tums) and given no recommendations on vitamin D. While that is changing, this particular study demonstrates how backwards this recommendation is.
In the study, researchers looked at 3448 men and 3812 women who were older than 50 years of age and broke them down into daily dietary calcium intakes of (1) less than 400 mg/d, (2) 400–799 mg/d, (3) 800–1199 mg/d, and (4) 1200 mg/d or greater. Overall, the average daily calcium intake was 470 mg/d.
They then measured bone density and compared it to average daily calcium intake. Here’s what they found:
- Those with calcium intake less than 400 mg/d had lower bone density (specifically, femoral cortical thickness and buckling ratio).
- In men, bone density was higher in those with calcium intakes up to 1200 mg/d.
- Importantly, these interactions disappeared when the 25-hydroxyvitamin D level was over 30 ng/mL (men) or 20 ng/mL (women).
So, while it can be argued that calcium is important for bone health, it pales in comparison to the effect of vitamin D, so much so that adequate (not even optimal) levels of vitamin D essentially protect against low calcium.
That’s not to say that you should deliberately deprive yourself of calcium while taking vitamin D just to see if it pans out. Rather, a solid diet with good calcium sources combined with vitamin D supplementation (starting at 2,000 IU / day) is the best way to go. Solid sources of dietary calcium include:
- Spinach and kale
- White beans
- Some fish like sardines, salmon, perch, and rainbow trout
- And there are foods that are calcium-fortified, such as soy milk, some orange juice, oatmeal, and breakfast cereal
You might notice the suspicious lack of dairy on the list. If you’re a regular reader of the Rantings you’ll know that I’m not a fan of dairy. Enough so that I compiled an eBook of research demonstrating that dairy is not the health food that we think it is that can be found by clicking here.
You have heard of the placebo response and have a general idea of how it works. The reality is that few of us know just how powerful it is.
This wouldn’t be a problem except that most drugs, when studied in clinical trials, are compared to placebo. This means that patient beliefs during treatment may have much stronger effects than the drug itself. Many drugs are studied under double-blind placebo controlled studies in the attempt to control for the placebo response. In these studies, neither the reviewer (many times this is the treating physician) nor the patient knows who is taking the placebo and who is taking the active drug. But if the patient even thinks he or she is on the active drug, it can completely through off the results of the study.
In single-blind studies, the reviewer knows whether or not the patient is on the placebo or drug. This requires the reviewer to maintain an absolutely neutral attitude towards the patient lest he or she gives a hint as to what arm of the study the patient is in.
In non-blinded studies, all bets are off.
Although I don’t have the reference I remember coming across a study on blood pressure medications. The sneaky design of the study had participants believing that the study was designed to compare the drug to the placebo. In the study, the placebo had a pretty powerful response and the drug response was only a little bit stronger. However, when researchers teased apart those who were most compliant with taking the pills, whether drug or placebo, had the strongest blood pressure response. From compliance, we can conjecture that those who took the pills as prescribed had a much deeper belief that it was going to help them. This belief trumped all as far as a treatment response.
With that being said about the power of placebo, the opposite can also be true. This is called the nocebo response and deals with patients who have negative expectations for treatment or side effects. In other words, if you hear from your doctor that Drug A has some pretty nasty side effects, you are actually more likely to experience said side effects.
This particular study will completely destroy your faith in the ability to truly study the benefit of any drug in any study.
In it, researchers took 66 chronic migraine sufferers and followed them from an initial migraine attack through the next 6 attacks. In each of the attacks (after the initial attack for which no treatment was given, which served as the control), participants were given either a placebo or Maxalt (10-mg rizatriptan) over the course of the next 459 attacks.
(Editor’s note: due to the nature of this article, I will not go into the correct approach to the management and elimination of migraines. Feel free to check out my Migraines and Epilepsy eBook for that…)
What made this trial different was what was communicated to the migraine sufferer. The treatment was given under three different information conditions:
- Negative—they were given and told they were given a placebo
- Neutral—they were given and told they were given Maxalt
- Positive—they were given placebo but told it was Maxalt.
Pretty clever (but sneaky) if you ask me. Here’s what the researchers found out:
- Response to Maxalt was stronger than placebo (not unexpected).
- The placebo response was stronger than no treatment (not unexpected either).
- The placebo, even when the patients were told it was a placebo, had a stronger response then no treatment (a wee bit of a surprise here…)
- When participants were given placebo labeled as (i) placebo, (ii) Maxalt or placebo, and (iii) Maxalt, the overall placebo effect increased.
- Maxalt had a similar progressive boost when labeled with these three labels.
- The response to Maxalt labeled as a placebo and placebo labeled as Maxalt were similar.
- Compared to no treatment, the placebo, under each information condition, resulted in more than 50% of the drug effect.
This is really interesting stuff. Basically, the more “positive” information the patient got, the stronger the response, regardless of whether it was a drug or placebo. The reverse was also true—if the patients did not believe they were given the drug the response was not as strong.
This says a few things about society and can help me as a physician. First, a note on society. And it’s a sad note. This study found that, even if patients were told they were given a placebo that we all know is “just a sugar pill” our programming that drugs “fix things” runs so incredibly deep that merely taking a pill has the potential to help EVEN when we know it can’t possibly help.
More importantly, I know that, as a physician, my beliefs and reassurances about the treatments I offer have a strong impact on the outcomes of these same treatments. My assurance to a patient that a treatment for his or her condition can be very effective can be as powerful as the treatment itself. Ironically, with experience and seeing thousands of patients over the years benefit, I become more confident in the treatment I provide. This confidence can, in turn, improve the outcomes of my patients. Pretty cool.
I have covered the topic of irregular heartbeats like atrial fibrillation and what you can do to fix the problem in previous articles.
A visit to your cardiologist will leave you with instructions to cut caffeine intake and stress and likely a prescription for a beta blocker and maybe a blood thinner if there is a higher risk of stroke. Ironically, the beta blocker will increase your risk of stroke (the very thing we’re trying to prevent) and diabetes (which can make a-fib worse).
At the heart of the problem is the heartbeat regulating cells firing before they are supposed to. It is an inability to STOP a heartbeat. The second heartbeat essentially begins in the middle of the first, throwing off the rhythm. The problem is that this can create turbulence in blood flow and turbulence can lead to a blood clot forming and being released towards the brain.
Luckily, there are ways to help your heart beat the way it is supposed to. The first approach involves my favorite organelle, the mitochondria. Improve the amount of energy available to the cells of your heart and they can beat when they are supposed to beat. They will have the energy to hold off from firing too early.
Another way to help your irregular heartbeat is to improve the health of your cell membrane. Each and every cell in your body has a cell membrane. The job of the cell membrane is to create a border between “inside” and “outside” of the cell. That way, stuff that is supposed to get in gets in and stuff that is not supposed to get in is kept out.
This creation of a boundary is incredibly important for a cell (brain cells as well as heart rhythm cells) to fire when it is supposed to fire and NOT fire when it is supposed to.
And this cell membrane is made up of fats. You can literally choose how well your heart and brain cells fire by the dietary choices you make. Good, healthy fats and things work the way they are supposed to. Eat crap and low quality fats and it can wreak havoc on cell function.
This particular study reinforces just how solid this relationship is.
The Mediterranean diet is known for its intake of healthy fats, most notably from olive oil, fish and nuts. These fats (provided it’s wild caught fish and raw nuts) will contribute to healthy cell membranes and better cell function. In this study, they divided 6705 participants who did not have atrial fibrillation into 3 diet groups:
- Mediterranean diet supplemented with extra virgin olive oil,
- Mediterranean diet supplemented with mixed nuts.
- Advice to follow a low-fat diet.
Over the course of an average of 4.7 years, the group was observed to see if anyone developed atrial fibrillation. Here’s how the diets played out:
- The Mediterranean diet with extra virgin olive oil cut the risk of developing AFib by 38%.
- The Mediterranean diet with nuts cut risk 11% compared to the control diet.
While this is not the end-answer for lowering your risk of developing an irregular heartbeat, but the types of fat in your diet clearly play a role. Combine this with stress management, exercise and a lower-calorie, higher phytonutrient diet and it’s going to be a stronger effect.
The take home message is that irregular heartbeats CAN and should be managed with lifestyle choices. It is a sign that something is wrong with the cells of your heart that needs to get fixed. Medications in no way fix the underlying problem.
Vaccination is one of the most hotly debated health topics there is. But rarely do either side of the debate understand the details.
The pro vaccine group has near-religious faith in the altruistic behavior of public health officials and the pharmaceutical companies. And, boy, if any of you think that profit is not a driver of the drug companies we really have no more room for discussion.
For me, just because “they” tell me I should turn my child into a voodoo doll replica in his first handful of years is not a strong enough reason to jump off the cliff with the rest of the lemmings. If I’m going to do something for my child’s health, there better be a damn good reason and very solid research behind it.
If the pro-vaccine group wanted to sound less like religious fanatics they could start by not blaming parents who choose not to vaccination their children for every outbreak of every disease on the planet and verbally trash their parenting skills.
They could also check their facts when they discuss Dr. Andrew Wakefield’s research and subsequent smear campaign when it came to his research on ileonodular hyperplasia and the combined MMR vaccine. Almost always the facts are ignored and the hype and publicity is regurgitated.
Rather, they should bring up the fact that some vaccinations have some good track records. Smallpox and polio might be on the list, although there are some strong opinions that suggest that public health measures played no small part in the near-eradication of these diseases.
The answer likely lies somewhere in the middle.
The anti-vaccination crowd will fall back on the autism debate and the components of the vaccination like mercury (despite what anyone says, it is NEVER a good idea to inject ANY form of mercury into the human body), formaldehyde, aborted embryos and a long list of nasty sounding chemical compounds.
While these may be valid points, it’s not the best stance for the anti-vaccination crowd. Rarely have I read through the inevitable discussions that follow an article on vaccination (whether pro or con) and was proud of either side.
As someone who considers themselves quite well read on the subject of vaccination I lean towards the anti-vaccination crowd. Part of the reason for this is that we really, really don’t know what we’re doing. Worse, the story of what is best continues to change.
As an example, the Prevnar vaccination for pneumococcal infections (pneumonia and meningitis) started out addressing just 7 strains of the bacteria. Over time, we realized that, like a giant wac-a-mole game, Mother Nature was increasing infections caused by other strains. These infections were more severe and more resistant to antibiotics. So they redeveloped the vaccine to include 13 strains and the recommendations when out for everyone who had gotten the 7-valent shot to come in and get the new 13-valent shot. What a financial windfall, huh?
Examples like this are everywhere, including this particular study.
In it, researchers looked at 279 school aged (5-15) children who saw a pediatrician for complaints of a persistent cough that had lasted at least 2-8 weeks. Vaccination status was gathered, including how long it had been since the child had his or her preschool booster. These kids were checked for pertussis infection. The results were a little eye-opening:
- A hefty 20% (56 children) had evidence of whooping cough.
- Of the 215 who had been fully vaccinated, 18% (39 children) had whooping cough.
- In the kids who had the booster at least 7 years ago, the risk of pertussis was more than three times higher (21/53 kids, or 40%) than the kids who had the booster within the 7 years (20/171 kids; or 12%).
A few things to point out here. First, there was little difference between vaccinated and unvaccinated kids in the rate of whooping cough (20% versus 27%). Seven percent difference is hardly something to hang your hat on.
Next, it is clear that despite frequent boosters, the whooping cough vaccine does not really provided any significant long-term protection. While this study is not large enough to address it, in most cases, an actual infection (versus the vaccination) provides a much more long-lasting and potent protection against an infection.
Lastly, I really think that, in contrast to what you hear in the press about a whooping cough resurgence, pertussis has been alive and well among us but just not recognized for what it was. Not, with an increased vigilance by pediatricians it seems like there is a large increase in the number of kids with whooping cough.
If this is the case, then whooping cough vaccination has really not been a strong player in keeping pertussis at bay in our society, although it would receive undo credit.
Boy did the 90’s screw us up. The USDA’s disease-causing pyramid let to some pretty ingrained misinformation about what leads to weight gain.
The emphasis on eating grains without any education about refined versus whole grains and using fats and oils sparingly was a move in the wrong direction. We replaced healthy oils like olive oil in foods and replaced them with refined carbohydrates like enriched wheat flour and high fructose corn syrup. There are few things you can do to sabotage your health more than follow this pattern.
Many of the more popular diet programs gave high emphasis on eating foods low in fat. Salad dressings with olive oil cost more points than high fructose corn syrup varieties. Low quality, highly processed frozen entrees have less points than unprocessed ones based merely on fat content. This is never something I would recommend.
Because of this, many of us, both old and young, have the misconception that eating fat will cause us to become fat. While this may be true for low quality fats like the saturated fat in corn-fed beef and fast foods as well as hydrogenated oils in the same fast foods as well as processed snacks like chips.
Just in case you still have any lingering doubts in the back of your mind that just maybe the USDA Dietary Pyramid should not have been scrapped, take a look at this particular article. In it, researchers overfed 39 participants with muffins that contained either saturated fatty acids (SFA-palm oil) or polyunsaturated omega-6 fatty acids (PUFA-sunflower). Liver fat, visceral adipose tissue (VAT-the bad kind), abdominal subcutaneous adipose tissue (SAT), total adipose tissue, pancreatic fat, and lean tissue (the good stuff) were all measured by MRI. Here’s what they found:
- Both groups gained similar weight.
- The SFAs, however, led to large increases in liver fat compared as well as a twofold larger increase in VAT (the bad stuff).
- On the other hand, the PUFAs led to a nearly threefold larger INCREASE in lean tissue (the good stuff).
Let me get this straight. Adding fat actually led to an increase in lean body mass?? How can that be possible when fat = fattening??
It actually make sense since healthy fat actually improves the cell membrane and allows the cells of our body to communicate better with one another. When this happens, hormones like insulin work more effectively at controlling blood sugar and keeping body weight under control.
That being said, I do have to say that sunflower oil would not have been my preferred choice for healthy fats. I prefer to keep omega 6 intake lower and omega 3 intakes higher. And my preferred source of omega 6 fatty acids would be nuts (raw—NO added oils) and olive oil.
Although, it IS tempting to run out and buy a large bag of high-oleic sunflower oil salt and vinegar potato chips and finish them in a single sitting and damn the 800 calories….
Having a child can be one of the most rewarding experiences in your life. But to go into pregnancy blindly can lead to a lifetime of problems for your baby.
This may sound a little drastic and maybe even a little far-fetched. Just stay away from drugs, don’t drink alcohol and stay away from nuclear reactors. Pretty simple.
Ok…so maybe decisions during pregnancy can play a role in your unborn child’s health and well-being. Maybe you’ll try to eat some more veggies this month and maybe cut back on the fast-food trips. That’s got to be worth a few IQ points in college.
But what about before you even get pregnant??? Could your dietary choices leading up to pregnancy influence the outcome of your pregnancy? And could these outcomes have lifelong impacts on your as-of-yet-unborn child?
Just by the fact that I’m asking these questions should give you the answers. But before we get into the details of this blog post, there are two things we should cover.
First of these is infertility. The largest cause of infertility in this country (70%) is polycystic ovarian syndrome, or PCOS. PCOS is, in almost every case, the result of poor lifestyle choices. Unfortunately, a visit to a fertility specialist is more likely to end up with you getting a prescription for Clomid to force fertility than it is for you to enter into a long discussion on healthy lifestyle changes with your “fertility specialist.”
This is a very wrong approach. For any couple with fertility issues the discussion on lifestyle needs to come first. Regardless of how fast your biological clock is ticking, a few more months of improving your lifestyle is worth every second.
Why? Because of the second thing we need to cover. Pre-term birth will increase the risk of obesity, diabetes and heart disease in your child decades down the line. Conceiving a baby through the use of assisted reproductive technologies (ART) like Clomid will increase the likelihood of having a pre-term birth. Not good.
So what else will increase the risk of having a pre-term delivery before 37 weeks? There are many factors like phthalate exposure (that “new shower curtain” smell from vinyls and plastics), inflammation in the vaginal vault (think yeast infections) or stress that can increase the risk of a pre-term birth.
According to this particular study, it turns out that your dietary choices PRIOR to pregnancy can influence your risk of having a baby go to full term. In it, researchers look at the dietary habits of 309 in the 12 month period prior to getting pregnant. There were 3 dietary patterns identified:
- High-protein/fruit (characterized by fish, meat, chicken, fruit, and some whole grains)
- High-fat/sugar/takeaway (takeaway foods, potato chips, refined grains)
- Vegetarian-type (vegetables, legumes, whole grains).
Based on this information, researchers looked at the odds of having a pre-term birth, having a shorter gestation period as well as birth length. Here’s what they found:
- Those women with the high-protein/fruit pattern had a 69% lower risk of pre-term birth.
- Those with the high-fat/sugar/takeaway pattern had a 54% higher risk of pre-term birth as well as a shorter gestation period and birth length.
Personally, I was a little surprised that the vegetarian type diet pattern did not score better, but this may have to do with the amount of protein available. Just because someone does not eat meat this does not make them a vegetarian.
That aside, here are some tips on lifestyle as you get ready for your pregnancy:
- Protein is important, but so are the choices of protein sources. Do your best to stick with organic chicken, wild-caught fish and grass-fed throughout the lifecycle beef. Good plant-based sources of protein include hummus, rice, beans and nuts. Chow liberally on the plant-based sources and try to limit your quantities of the animal based proteins.
- Fruit is also a good idea, but don’t limit yourself to the basics. Melons, apples and oranges are good, but don’t forget pomegranate, wild blueberries, strawberries, kiwi and blackberries. Stay away from the juices—they’ve got way too many calories for the nutrition they provide.
- Whole grains do not just mean wheat. Quinoa, amaranth and rye are all powerhouses in their own right. Experiment with the test of other, more ancient, grains. And absolutely NO enriched wheat flour.
The list could grow much longer, but these are some recommendations to go along with the dietary patterns found in this study. Overall, though, you (meaning your AND the impending father) need to understand that this is NOT about you. Every choice you make, leading up to pregnancy, during pregnancy and during the first years of your little ones’ life, will have an impact on his or her risk of chronic disease decades in the future.
The cholesterol story continues, but the emphasis placed on total cholesterol is finally fading. Now the heat is up on HDL, or the “good” cholesterol.
It’s almost sad that, after years and years of promoting high cholesterol as a risk factor for heart disease, the medical community has quietly backed off from this mistaken belief that total cholesterol is linked to heart disease. I should probably clarify that. Mainstream medicine has finally backed off from the idea of artificially lowering your total cholesterol with drugs actually saves lives.
It is true that those with high cholesterol are at an increased risk of having a heart attack and dying of cardiac causes. But lowering cholesterol with a drug like Lipitor or Crestor is just short of worthless. Lowering total cholesterol with lifestyle, however, will absolutely, positively save your life.
Listening to the commercials for drugs to lower cholesterol, you will no longer here the announcer list “high cholesterol” as a risk factor for heart disease. What a massive kick in the gluts. The drug that was developed to lower cholesterol should now not be used solely to lower the high cholesterol is was designed to affect. Kind of makes your head spin.
HDL, also called “good” cholesterol, was in the spotlight for a while. Since it is clear that low HDL cholesterol is bad for the heart and higher levels protected against heart disease the drug companies spent millions of research dollars to develop a drug that would raise HDL levels. They all failed miserably, actually increasing the rate of heart disease in clinical studies. For now, the research along these lines has halted (at least as far as I know…).
But this does not mean that higher HDL levels do not have an effect on heart disease. They clearly do. It’s just that the HDL molecule is far, far more complex than we ever imagined. It is actually a group of molecules, NOT a single molecule. Positive lifestyle choices will affect the entire class of HDL molecules, sending the protective HDL molecules higher and the less protective ones lower.
One thing that is well-known about HDL is that it can act as an antioxidant and an anti-inflammatory molecule. This is a good thing. It may also mean that, should you suffer a heart attack, the HDL molecule can swoop in an lessen the damage done.
You see, when you have an ischemic heart attack (or stroke, for that matter), the area that loses blood supply and dies off (called the infarct) is actually smaller than the total area that ultimately gets damaged. This means that, if the original area that loses blood supply is the size of a dime, by the time it’s all done, the tissue damage area in the heart may be the size of a quarter. We can all agree that less heart damage is a good thing.
This particular study gives those of us with low HDL levels an idea of how we can protect our hearts in the event of a worst-case scenario. Researchers looked at mice with the inability to produce Apolipoprotein a1 (apoA1). ApoA1 is a main component of the HDL molecule. So higher apoA1 can mean better protection in the event of a heart attack. It turns out that in the mice who could not produce apoA1, the damage to the heart was 125% larger than normal mice in the event of an ischemic heart attack.
However, when the researchers gave coenzyme Q10 (CoQ10) to the mice who could not produce apoA1, the extra damage went away. A simple supplement that supports the ability of a cell to generate energy could make the difference between life and death. In the normal mice, though, CoQ10 did not make a difference in the size of the damage.
Based on this, some of you may be throwing good money away (CoQ10 is expensive–you can check out some of them on Amazon by clicking here) if you are taking CoQ10 to protect your heart and your apoA1 levels and HDL levels are not low. On the flip side, if you have lower HDL and lower apoA1 (this value can be checked on a standard blood panel), it might be a very smart idea to begin supplementing with 50-100 mg of good CoQ10 daily.
An important note to add here. The statin class of drugs to lower cholesterol are notorious for also lowering levels of CoQ10 (CoQ10 and cholesterol are on the same metabolic pathway and are both blocked by these drugs).
Does this mean that patients with low HDL who are put on statins may actually have WORSE outcomes after a heart attack??? If this turns out to be true, this would be completely ironic since “low good cholesterol” is now one of the indications for giving someone this worthless class of drugs.
We live in a toxic soup. In an attempt to avoid at least SOME of the pollutants, many have become dilligent about avoiding Bisphenol A (BPA) in plastics.
I first wrote about BPA in canned goods as early as 2001 and have been a vocal advocate for avoiding its use as much as possible. It took some time and pressure from consumers, but the plastics community responded by coming out with everything in a BPA-free version. It’s now widely accepted (by everyone EXCEPT the EPA) that BPA is bad for our health and you will see no labels on the front of baby bottles proudly proclaiming that they still load their plastics with BPA.
Birth defects, diabetes, obesity and some cancers have been linked to BPA exposure. The scary part is that almost all of us have detectable levels in our bloodstream. Exposures are everywhere and can include:
- Plastic water bottles
- Food can liners
- Credit card receipts
- Aluminum can liners (in the study referenced above on register receipts, one participant had to be excluded because, after drinking 4 canned sodas, his BPA levels were 27 TIMES higher than everyone else in the study)
So you educate yourself on your exposure sources of BPA and decide to only go for the BPA-free water bottles and baby bottles. This is a good thing, right?
I have always been wary of plastics in general and specifically plastics well-known to contain BPA. For my family, we only use stainless steel pitchers for our tea (you can find the ones we use on Amazon by clicking here). We try to cook in glass Pyrex dishes whenever possible. We rarely drink bottled water (ours is a very heavy tea drinking household). While I don’t have a problem with sparkling waters (like La Croix or Perrier), these aluminum cans are lined with BPA so we avoid them. In its place we have just ordered the Soda Stream Crystal, which uses glass bottles (again–this can be found on Amazon by clicking here). I’ll have more feedback on how it works in a few weeks.
In general, I have an inherent distrust in plastics, BPA-free or not. Turns out that my paranoia may actually be somewhat rationale, despite what the EPA states…
This particular study looked at the hormonal action of other chemicals present in BPA-free water bottles that have been used to replace the bisphenol A. Here’s the details:
- The study looked for estrogenic activity in the compounds now found in BPA-free water bottles.
- These chemicals included acrylic, polystyrene, polyethersulfone, and Tritan™ resins.
- Unstressed and stressed (plastics worn out from heating or handling or sun exposure) both leached chemicals that messed with estrogen receptors.
- This included products made for use by babies.
- UV radiation had a tendency to increase the leaching of chemicals with estrogenic activity.
- However, some BPA-free PC-replacement products made from glycol-modified polyethylene terephthalate (say that 3 times fast…) or cyclic olefin polymer or co-polymer resins did not affect estrogen receptors.
Overall some pretty scary results that should have you concerned. Maybe my paranoia is not really paranoia, but a distrust based on knowledge about environmental exposures. And I’d much rather prefer to consider myself ahead of the curve than wacky.
Medicine has created an imaginary divide between sickness and health. We described health as merely the absence of an identified disease.
In other words, you have heart disease or you don’t. You have cancer or you don’t. You have celiac disease or you don’t. Admittedly, over the years we’ve gotten better by identifying “pre” states. Pre-hypertension. Pre-diabetes. Pre-osteoporosis. Pre-cancerous.
These “pre” states were created less to educate you about needing to make better choices and more to identify the point at which the benefits of medicating a condition outweighs the risk of side effects. Just in case you think this sounds cynical, read up on the history of osteopenia (“pre” osteoporosis). It’s a little scary to see how much we all are duped by the drug companies when it comes to our health (NPR has a great overview of the process that went into building a drug market for osteopenia).
There is nothing wrong with using the label of “pre” when it comes to chronic disease. I use it all too frequently with prediabetic patients in my office. But to me, the “pre” is a warning sign that you need to get your act together because you are well on your way to any number of chronic diseases. We should NEVER rely on drugs for any type of “pre” condition. Never. Lifestyle changes are the only recommendation that should be on the table at this point. It is up to you to make the right choices.
One condition that we do not generally tack the “pre” label on is heart disease. Sure, we love to tell patients they are at risk because they have high cholesterol or high blood pressure or not exactly optimal body weight. But again, I think patients view this as an “off or on” situation. Just because you have high cholesterol does not reaaallly mean that you have heart disease. It only means that you are at a greater risk of having a heart attack.
This is an outright misunderstanding of the way heart disease works in our body. Having a heart attack or stroke is merely the end process of decades of abuse on your blood vessels. Almost the proverbial straw on the camel’s back. Would you make needed changes if you knew you were a single straw away from the end of your life?
Some still would not, thinking that they would be lucky enough to escape this outcome.
With that in mind, I would like to bring your attention to this particular study. In it, researchers looked at 405 men and 813 women with three important factors:
- They had, for some reason, suspected coronary artery disease.
- They had NO previous history of coronary artery disease.
- They had no evidence of coronary artery disease on cardiac stress testing.
You may very well match this group of participants. These patients would essentially have been given a clean cardiac bill of health after the tests were negative. But the researchers didn’t stop there. They looked at how well the blood flow moved through the coronary arteries using more specialized testing. Here’s what they found as they followed this group of patients over the next 1.3 years:
- 51% of men and 54% of women demonstrated some type of damage to their coronary arteries.
- For every10% increase in coronary flow reserve (basically healthier blood flow to the heart muscles) there was a 20% drop in the risk of major cardiac events.
- In a small group who were evaluated in more depth (307 women and 97 men) who had no hardening of the heart arteries on CT scanning 44% of men and 48% of women still had damage to the heart vessels.
In other words, these patients, who had normal cardiac testing, were well on their way to having a heart attack. And this was a large chunk of the patients in the study. I’m sure that these patients thought that “everything was ok” and continued to go about their merry little life thinking everything was peachy-keen.
We need to understand, as a society, that a very large chunk of us are already on the “pre” heart disease pathway and that damage to the very blood vessels supplying the critical nutrients and oxygen to the muscles of our heart is already occurring. Until we change our attitude towards heart disease and understand that it is a spectrum heart disease will continue to be this country’s #1 killer.
It’s been awhile since I’ve written about how much statins suck, so I thought I’d throw another article about the side effects of statins out there.
Basically, I just can’t figure out why we still use this class of drugs. At preventing a first heart attack (referred to as primary prevention) you have to treat 1000 people for 5 years to prevent 11 heart attacks. During this time, another 8 out of the 1000 will develop diabetes. Another huge chunk of this group will experience a long list of other side effects like muscle pains, muscle damage and liver problems just to name a few. With all of this taken into account, many in the cardiology community think we should be giving MORE patients statin drugs.
Am I the only one that paid enough attention in math class to know that these numbers suck? There just really isn’t any other way to describe them. These numbers are so bad that we have to tell doctors and patients alike the numbers in a different way. We have to give the benefits in relative risk reduction (50%), not the absolute risk reduction (1%). I have covered this “playing with numbers” in previous blog articles so I won’t go into it in detail here. Suffice it to say that, in a group that is at an overall low risk of having a heart attack in the next 5 years (as would be a 45 year-old active male with elevated cholesterol) cutting that low risk in half (the 50% relative risk reduction) is not really going to make much of a difference.
All of this aside, I think the greatest dangers of all drugs, but particularly the statin drugs, is complacency. It is living with the idea that your condition is “controlled” with medication. That your health is somehow safer now that you’re on a medication. While this daydream is very, very clearly not true (as we see time and time and time again in the medical research) it seems like patients become less proactive in their health decisions because numbers are “improved” on a drug.
So if your cholesterol is lowered by taking a drug to lower cholesterol (which it most likely will be because these drugs do actually lower cholesterol quite well) you may not be quite as motivated to avoid refined carbohydrates, avoid animal saturated fats and eat more omega-3 fats in your diet. Previous research has already demonstrated that statins users have lower diet quality than non-statin users (more fats, high caloric intake and a higher BMI).
Just to take this proof of concept one step further, this particular article looks at the activity level of statin users versus non-statin users (using the Physical Activity Scale for the Elderly, or PASE score) in a group of 5994 men aged 65 years and older. And it’s not pretty. Here’s the details:
- Statin users had lower PASE scores than non-users.
- For new statin users, the annual PASE score declined at a faster rate than nonusers.
- Statin users expended less METs (they basically burned less energy).
- Statin users engaged in less moderate physical activity (about 40 minutes less per week).
- Statin users engaged in less vigorous activity and had more sedentary behaviors.
I think it would be pretty easy to argue that, in those with some degree of cardiac risk, regardless of what we are measuring (cholesterol, body weight, HDL, hsCRP, etc…) MORE exercise should be the norm. So why do statin users seem to be adopting poorer lifestyle choices and exercising less? Maybe it’s because the muscle pain and cramping side effects are cutting down exercise time. If so, this is unfortunately because exercise is far more powerful in preventing heart disease on a bad day as statins are on a good day.
Or is it that statin users become complacent, adopting the attitude that they really don’t need to make changes because the drug is going to do the work? If so, this is a very dangerous and slippery slope for your health.