Ingredient in makeup could bring on early menopause?

The research is new, so this may or may not bear out over time. But right now the suspicion is that phthalates, a common ingredient in makeup and in household cleansers (?! – I’m putting something on my face that I use to clean my toilets or something?) may bring on early menopause. And that’s bad news because early menopause brings on osteoporosis. From the article:

In the study, Grindler and her colleagues examined the levels of phthalates in the blood or urine of 5,700 women. Those with the highest amounts were found to have gone through menopause an average of 2.3 years before the others. Menopause typically occurs in women around the age of 51, so those exposed to the highest levels of phthalates were going through it at around age 49.

But Grindler told those at the conference that some women may be reaching menopause 15 years early, in their mid-30s. She suggested that the women may not only have been exposed to phthalates through makeup, but also through the eating of more packaged foods.

Phthalates also have been cited as the culprit in other studies looking at risks for cancer, obesity and diabetes. In one recent study, phthalates were tied to reproductive system abnormalities in mice.

Researchers at Washington University emphasized that the studies are still in the preliminary stages and that final results of won’t be released for months, noting that they “don’t want to scare people.”

Wait a second. This is ringing some kind of bell. Wasn’t there an article awhile back about how people who cleaned their houses more often had a higher incidence of cancer?  Was that it? I remember joking that it was a good thing that I was such a pig. So could this all be related?

Breast cancer drug found to cause significant bone loss.

Its name is Exemestane (also known as Aromasin). The drug is already widely used to prevent recurrence of breast cancer. But they’ve been looking into using it as a preventative. (I’m guessing that if there’s a family history of breast cancer, perhaps they were thinking of prescribing this drug to woman at high risk for developing breast cancer in hopes of keeping them from getting breast cancer. The article says it reduces the risk of getting breast cancer by 65 percent.)

Tamoxifen and raloxifene are already approved for breast cancer prevention, but blood clots are one of the big side effects from those two drugs.

Dr. Angela M. Cheung, the lead investigator of the new study, said its findings should not discourage women at high risk of getting breast cancer from considering the drug. From the article in The New York Times:

“Sometimes the options are, ‘Should I take my breasts out, or should I take a medication such as this?’ ” said Dr. Cheung, who is director of the osteoporosis program at University Health Network in Toronto.

The new study is actually a more detailed evaluation of bone quality in 351 of the 4,560 postmenopausal women participating in the study published in June. The women were evaluated by a relatively new technique called high-resolution peripheral quantitative CT. After about two years, the researchers found, those who were taking exemestane had an average 6.1 percent decline in the bone mineral density in the wrist, compared with 1.8 percent in decline for women getting a placebo.“

I’ve talked on here before about high-resolution peripheral quantitative CT (or QCT) before. It is a much more accurate way to measure bone density (especially for people with smaller bones) because it’s a three-dimensional measurement. So that 6.1 percent decline is… real. But beyond declining bone quantity, it seems that the quality also suffers:

“The exemestane users also had more evidence of a weakening of bone structure. That suggested that conventional bone density tests may not be able to detect all the damage caused by the drug, the researchers said.”

What a choice! Door #1 has cancer, door #2 has blood clots, door #3 has weak bones. I suppose when doing the math, one thing to consider might be how are you bones before the drugs and how long are you expected to be on them? Is it for life? Or five years? The drug works by inhibiting aromatase which in turn lowers estrogen levels (mystery solved on why it reduces bone density.) How much is 6.1 percent loss? I think it depends on the g/cm2 measurements, but to give you a rough idea, my gain of 0.20 points in my hips translated to a 3.7% gain. My gain of .20 points in my overall-spine translated to a 7% gain. So it could be a little  (o.20 points) or it could be a lot-ish (.40 points.)  If you only had to be on the drug a couple of years, for an overall bone density loss of .40 points on your DEXA, that doesn’t seem like that much of a tradeoff. But long term? I don’t know.

What do deer antlers and bones have in common?

photo: thinkrockpaperscissors.com

Both need calcium in order to grow and remain strong. Scientists noticed that some deer have antlers that snap off or break, while other deer are able to grow a rack of antlers that hunters’ envy. (I’m not sure which is worse: broken antlers or a bullet…I digress.)

The Research Institute for Hunting Resources (RIHR) decided that the broken antlers and osteoporosis could be linked. So they studied the antlers and discovered that the broken-antler deer were not low in calcium, but were low in manganese, one of those minerals that helps the body absorb calcium. According to the article in ScienceDaily:

… “previous antler studies show that manganese is necessary for calcium absorption. Our hypothesis is that when the human body absorbs less manganese or when it is sent from the skeleton to other organs that require it, such as the brain, the calcium that is extracted at the same time is then not properly absorbed and is excreted in the urine. It is in this way that osteoporosis can slowly strike.”

* * *

“Antlers grow by transferring 20% of the skeleton’s calcium towards their structure. We therefore saw that it was not calcium deficiency that caused the weakening but rather the deficiency of manganese,” clarifies Landete. “The lack of manganese was almost as if the ‘glue’ that sticks calcium to antlers bones was missing.”

This is a new hypothesis and the research is just beginning. But it’s intriguing. Manganese is one of those minerals that the brain needs an abundance of as well. Our skeletons and our brains are fighting for the manganese stores in our bodies. And if true, this hypothesis could explain another phenomenon: the link between development of osteoporosis and then subsequent development of diseases like Parkinson’s and Alzheimer’s.

The exhaustion of manganese reserves could be behind the bone disease and the cerebral degeneration. “We are collecting human bones to confirm this. However, studies on rats in which Alzheimer’s disease has been induced by aluminium intoxication show that as the severity of this disease increases, manganese levels in the bones decrease,” says Landete.

So by now you’re maybe wondering what to eat to get more Manganese. It’s plentiful in spinach, spelt, pineapple, cloves, cinnamon, oats, pumpkin seeds and brown rice. You can read more about manganese here and find a chart (at the bottom) with various foods’ amounts of the mineral.

Gluten Free is going Mainstream

In the Sunday Times Magazine, there’s a great article called “Should We All Go Gluten Free?” It is a fascinating history of celiac disease and the rise of gluten-free products in America. Did you know that until 1999, celiac was believed to be a mostly European disease, and the estimates for the number of Americans with celiac were placed at 1 in 10,000. A doctor from Italy, Dr. Fasano, who was practicing at the University of Maryland thought that figure had to be off. After all, where do the bulk of Americans come from? Europe. (Well. Not anymore.  I believe Puerto Rico and Mexico are fast catching up.) So this doctor did an informal blood study — he randomly took 2000 blood samples and tested them for celiac and found that 1 in 250 had the disease. So then he decided to do a crazy large study (13,000 subjects in 32 states) and the number went up to 1 in 133 with the disease. Young people are being diagnosed at a rate of 1 in 5.

1 in 5?!!

Bad news for a lot of bones out there.

The silver lining is that General Mills (who we know is  a huge food conglomerate) is jumping on the gluten-free bandwagon. Gluten-free Chex cereal, gluten free Betty Crocker mixes, gluten free icing, gluten free pancake mixes, gluten free soups. It’s a really interesting article. And again, it makes me wonder whether I should get tested again. (The last time I got tested might not have been so accurate because I’d been trying to do without gluten for weeks prior to being tested. You have to eat it long enough for the antibodies to build up in your blood.)

You can give the article a read here.

Want to avoid heartburn? Don’t eat near bedtime.

You’ve probably heard your mother or a friend say that a bajillion times. But is it true? Evidence seems to suggest it is. Avoiding eating between 3 and 4 hours prior to bedtime really does reduce heartburn.  Heartburn / acid reflux — any steps you can take to reduce them that don’t involve medication is good. Because PPIs contribute to bone loss.

So much for the alkaline diet theory.

From Denise Minger of Rawfoods.com, the person who turned the China Study on its head, comes this report that dietary calcium in the form of dairy does not leach calcium from your bones, nor does eating animal protein. Humminah-wah?

Like most things that make good headlines, the actual research is much more subtly nuanced and I recommend you read the entire article. At the risk of getting in trouble, I’m going to paste the whole thing here, because you’d have to scroll down the article past a bunch of stuff about cholesterol and heart health to get to the bone stuff, which might lead you to think I posted the wrong link.  (But in case you want to read about the entire China Study debunking, here’s the link.) Thank you, Betsy, for bringing this to my attention. Fascinating!

Dietary calcium and bone density among middle-aged and elderly women in China (PDF) by Ji-Fan Hu, Xi-He Zhao, Jian-Bin Jia, Banoo Parpia, and T. Colin Campbell.

True to its title, this paper examines the role of calcium in bone density in the China Study data—with a special focus on the effects of dairy calcium versus plant calcium. Campbell et al. zoomed in on five counties with “distinct lifestyles and diets”: the dairy-and-meat-loving Xianghuangqi, the infamous dairy-full Tuoli, and the rural, nearly-vegan farming towns of Jiexiu, Cangxi, and Changle.

But before we look at the paper itself, let’s see how Campbell summarized its findings in a Cornell Chronicle article in 1994:

Animal protein, including that from dairy products, may leach more calcium from the bones than is ingested, said Campbell, professor of nutritional biochemistry at Cornell and director of the Cornell-China-Oxford Project, the most comprehensive project on diet and disease ever conducted.

Campbell [and other collaborators] analyzed the role of dietary calcium in bone density by following closely the diets of 800 women from five counties that have very different diets in China. … Analyses of these data suggest that increased levels of animal-based proteins, including protein from dairy products, “almost certainly contribute to a significant loss of bone calcium while vegetable-based diets clearly protect against bone loss,” Campbell reported.

Sounds pretty clear: The dairy-eating counties must have had poor bone health due to their animal protein habit, whereas the more plant-based dieters were skeletally superb. In other words, milk does a body bad! But do the summaries above match up with this paper actually found? First, let’s look at what the women in each county were typically eating:

*Lest I get the “you’re trying to justify your dairy addiction” line and/or accusations of dairy industry affiliation, I’d like to remind everyone that dairy hasn’t been part of my diet in over six years, and I believe the dairy most people consume (low-fat, ultra-pasteurized, etc.) is downright nasty stuff. But that doesn’t mean I won’t defend dairy when the science warrants it.

As you can see, Xianghuangqi ate a pretty shabby diet as far as whole-foods veganism is concerned: We’ve got dairy galore, beef, mutton, wheat flour, a mere smattering vegetables, and millet. Their bones should be snapping like peanut brittle! Tuoli’s not much better, what with their milk tea, animal flesh, and decided lack of green leafy veggies. More bone snappage, right?

I’ll let the paper speak for itself:

Analysis by individual for all counties combined showed that [bone mineral content] and [bone mineral density] were correlated positively with total calcium (r = 0.27-0.38, P < 0.0001), dairy calcium (r = 0.34-0.40, P < 0.0001), and to a lesser extent with nondairy calcium (r = 0.06-0.12. P = 0.001-0.100), even after age and/or body weight were adjusted for. The results strongly indicated that dietary calcium, especially from dairy sources, increased bone mass in middle-aged and elderly women by facilitating optimal peak bone mass earlier in life.

Did you catch that? Dairy calcium—far more than plant calcium—was linked with stronger bones. Moreover, the paper notes that “nondairy calcium … showed no association with bone variables after age and/or body weight were adjusted for.”

Continuing on:

Comparison of results in Table 7 reveal that calcium from dairy sources was correlated with bone variables to a higher degree than was calcium from the nondairy sources, probably resulting from the higher bioavailability of dairy calcium.

A comparison of the bone mass of women in the five counties revealed that 20% greater bone mass at the distal radius was observed for all age groups of women in county YA [Xianghuangqi], a pastoral county with high consumption of dairy foods, as compared with the nonpastoral areas with lower calcium intakes.

I’ll add my own unsolicited 2¢ and speculate that calcium probably wasn’t the only protective factor in the dairy-eating counties. Aged cheese, likely consumed at least in Xianghuangqi, is high in vitamin K2—a nutritional superstar when it comes to bone health (among other things). K2 isn’t present in plant foods except for a fermented soy product called natto (not everyone’s cup o’ tea). As the paper notes, the dairy-eating counties also had a higher intake of fat (25% of daily calories, opposed to 9.9 – 13.6% for the other counties), potentially increasing the absorption of fat-soluble vitamins necessary for bone health.

So how did Campbell conclude from this study that “increased levels of animal-based proteins, including protein from dairy products, almost certainly contribute to a significant loss of bone calcium”? The dairy part is unfounded no matter which way you spin it, but the rest of his statement probably stemmed from this:

The associations between bone mass and other nutrients, like dietary protein and phosphorous, were also examined. However, none of these nutrients showed an association with bone mass as significantly as did dietary calcium, although an inverse correlation was observed consistently for nondairy animal protein.

Unfortunately, that’s the only blurb in the entire paper that mentions animal protein in relation to bone mass, so we can’t see the data behind the “consistent inverse correlation.” In the context of this study, though, it makes sense: Protein has a complex relationship with bone formation, serving as a synergist when calcium intake is adequate, but as a potential antagonist when calcium intake is low. In other words, the effects of protein on bone health depend on how much calcium you’re taking in.

So for the counties in this study that ate more animal protein but sparse calcium—such as Changle, which had the highest non-dairy animal food consumption and also the lowest calcium intake (averaging a mere 230 mg per day)—I wouldn’t be surprised if an animal protein/weaker bones connection showed up. Whether that trend would hold at higher calcium intakes is a different story. And either way, this finding doesn’t jive with most other research done on this topic: Most studies show a protective association between animal protein and bone density, formation, and retention:

• Prospective study of dietary protein intake and risk of hip fracture in postmenopausal women. “Protein from animal sources was the nutrient variable with the strongest negative association with risk of hip fracture in this prospective study of Iowa women. Protein from vegetable sources did not appear to protect against hip fractures.”
• Effect of Dietary Protein on Bone Loss in Elderly Men and Women: The Framingham Osteoporosis Study. “Contrary to expectations, elders with animal protein intake up to several-fold greater than the RDA also had the least bone loss after controlling for known confounders. Nonanimal sources of protein were not related to BMD. These results suggest that typical population intakes of animal protein, within the range commonly consumed, do not result in bone loss. Rather animal protein intake appears important in maintaining bone or minimizing bone loss in elderly persons.”
• Protein Consumption and Bone Mineral Density in the Elderly. “Multiple linear regression analyses … showed a positive association between animal protein consumption … and BMD. Conversely, a negative association between vegetable protein and BMD was observed in both sexes. … This study supports a protective role for dietary animal protein in the skeletal health of elderly women.”
• Controlled High Meat Diets Do Not Affect Calcium Retention or Indices of Bone Status in Healthy Postmenopausal Women. “Calcium retention is not reduced when subjects consume a high protein diet from common dietary sources such as meat.”
  

In addition, if animal protein was such a bone-killer and plant protein was bone protective, we’d see vegetarians or vegans having the best outcomes in the bone department. But this just ain’t the case. At best, non-meat-eaters are equally matched with their omnivorous counterparts; at worst, they’re more prone to fracture:

• Veganism and osteoporosis: A review of the current literature. “The findings gathered consistently support the hypothesis that vegans do have lower bone mineral density than their non-vegan counterparts.”
• A Comparison of Bone Mass Measurements of Vegetarians and Omnivores. “In this review of 9 cross-sectional and 1 longitudinal study, little statistical significance between bone density and bone content was found between vegetarians and omnivores.”
• Effect of vegetarian diets on bone mineral density: a Bayesian meta-analysis.“The results suggest that vegetarian diets, particularly vegan diets, are associated with lower BMD, but the magnitude of the association is clinically insignificant.”
• Long-Term Vegetarian Diet and Bone Mineral Density in Postmenopausal Taiwanese Women. “Long-term practitioners of vegan vegetarian were found to be at a higher risk of exceeding lumbar spine fracture threshold … and of being classified as having osteopenia of the femoral neck.”

So, although the “calcium-leeching” properties of animal protein is a common battle cry in the vegan world, the research just doesn’t support it. There are even some interesting (and peer-reviewed!) papers out there looking at how belief systems influence the interpretation and misrepresentation of bone/protein studies. Read that link because it’s awesome.

But back on topic. This paper, with Campbell’s own name on it, suggests a strongly bone-protective role for dairy in the diet. Not quite the message we heard in “The China Study.”

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So that’s a lot of food for thought. In some ways it makes me sad — I’d like to think avoiding certain foods is the magic bullet for my weak bones. In other ways it makes me happy. I can enjoy my mac-n-cheese in peace.

Conflicting studies on gut serotonin and bone growth

Sometime last year (maybe it was the year before) I did a post on how a scientist (Dr. Karsenty) had discovered that mice who had too much gut serotonin had weaker bones. It went something like this:  humans with a genetic mutation that turns off something called LRP5 have very weak bones — so weak many cannot even walk. Dr. Karsenty genetically modified a bunch of mice to turn off / inactivate LRP5 and then observed that the mice had four to five times the normal level of gut serotonin. He then found that when he blocked gut serotonin production, the mice developed denser bones. And so the race to develop a drug that would block gut serotonin and thereby cure osteoporosis was born.

Well, hold on to your prescription pad because a new study has just been published that refutes all of those findings. In this study led by Dr. Matthew Warman, they found that gut serotonin levels had no influence on mice bone density at all.

[Dr. Warman's] group tried, but failed, to find that LRP5 has an effect on blood serotonin levels in mice or that those levels have a strong effect on bone.

When his group made mice with overactive LRP5 genes, the mice did make too much bone, but this had no effect on their serotonin levels. And when his group studied mice with inactivated LRP5 genes, the mice had weak bones but no increase in production of gut serotonin.

Dr. Warman and his colleagues also conducted a reverse experiment, producing mice that made very little serotonin in their intestines. They saw very little effect on the animals’ bones.

So whom to believe? The article concludes by saying the two teams used somewhat different methods to modify the genes they were studying (the LRP5), used different methods for measuring serotonin levels and different methods for measuring bone density. (Oh, why can’t labs all be consistent?)

I am a hardened skeptic, okay? But the fact that there is a drug company behind the research of one of the doctors (Karsenty) makes me lean ever-so-slightly in the direction of Dr. Warman.

BUT some scientists (besides Dr. Karsenty) believe SSRIs (anti-depressant medications like Paxil) work by raising gut serotonin levels, and we know (definitely know, not sorta think) that SSRIs cause bone loss. So I don’t know whom to believe. Doesn’t matter because I’m not taking any of those drugs. [Thanks for the link, Betsy!]

Proton pump inhibitors increase fracture risk

So says an article in The New York Times. We have talked about this on Bone Architect before, but I guess additional studies are ongoing, and each one adds to the pile of proof that some acid reflux medications are very, very bad for bones. The article states that the increased fracture risk does not apply to older acid-reflux medications called histamine-2 receptor antagonists.

Just how much does PPI (Proton Pump Inhibitor) use increase fracture risk? Twenty-nine whopping percent. Meaning you’re almost a third more likely to fracture if you’re using PPIs. People on long-term PPI use had a 30% higher chance of fracturing, and people on higher doses were — take a deep breath – 53% more likely to fracture. Holy broken femur, Batman!

It is believed that PPIs interfere with the intestine’s ability to absorb calcium.

By the way, there were some studies back in 2005 that showed acupuncture was effective at reducing acid reflux by 40%. Insurance often covers acupuncture. Perhaps give it a shot?

Coffee drinking; it’s genetic.

According to this study. See? I can’t help it! I was born this way!

Get the lead out!

Our dear Pam sent me a link today to an article reporting on the association between lead exposure and osteoporosis. They’re connected.

Evidently to your body, lead and calcium look a lot a like. So your body absorbs the lead and the lead in turn kicks out the calcium. 95 percent of the lead we have in our bodies is stored in our bones. And once it’s in there, it takes as long as 25 years to get it out. The article says doctors were slow to figure out that lead was a danger to bone health because pre-DEXAs, physicians used to measure bone health with x-rays. And because lead is denser and x-rays don’t pass through lead as easily, the lead-laden-osteoporotic bones did a bang-up job of looking like perfectly healthy bones when they were x-rayed.

But besides lead doing a “body snatchers” number on your calcium, there’s more:

…[T]he team’s most significant discovery has to do with a gene known as sclerostin and its ability to permit lead to cause bone loss.

Sclerostin is a potent inhibitor of bone formation: it keeps bone growth in check. But when lead interferes with this inhibitor, Puza says, something dramatic occurs.

“Lead exposure in the laboratory, in animals, and in humans drives sclerostin levels sky high,” he says. “If lead stimulates sclerostin and sclerostin is an inhibitor of bone formation, that’s probably preventing the normal bone from being formed. And that’s why over time you end up with not enough bone formation and a low bone mass.”

A drug that blocks sclerostin is being studied, Puzas says, which might help treat lead-related osteoporosis, but more research is needed.

Ugh. I think I mentioned our apartment building was sold to a new manager-developer. He’s got some crew in there ripping apart every vacant unit, and combining units, etc. But he’s doing everything on the cheap, so his crew isn’t exactly in the NYC Health & Safety Construction Crew of the Year book. There is dust flying everywhere. We’re pretty sure it’s loaded with asbestos because of the age of the building. So up until now I’ve been worried about lung cancer. Guess I’d better add osteoporosis via lead poisoning to the list as well. Should I start undergoing chelation? Or just eat a lot of broccoli?

By the way, the darker (or whiter) lines on the x-ray above are where the lead settled into the bones. Scary, huh?