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I advocate consumption of cold-water fatty fish a couple times per week for long-term protection against heart and brain disease. The protective component of fish may be the omega-3 fatty acids.
On the other hand, much seafood is contaminated with mercury, which can be toxic. So, is the mercury in fish actually toxic to brain tissue of folks eating reasonable amounts of fish?
A recent autopsy study answers, “No.”
Read further for details.
From the Journal of the American Medical Association, 2016 Feb 2;315(5):489-97. doi: 10.1001/jama.2015.19451. “Association of Seafood Consumption, Brain Mercury Level, and APOE ε4 Status With Brain Neuropathology in Older Adults.”
IMPORTANCE:Seafood consumption is promoted for its many health benefits even though its contamination by mercury, a known neurotoxin, is a growing concern.
OBJECTIVE:To determine whether seafood consumption is correlated with increased brain mercury levels and also whether seafood consumption or brain mercury levels are correlated with brain neuropathologies.
DESIGN, SETTING, AND PARTICIPANTS:Cross-sectional analyses of deceased participants in the Memory and Aging Project clinical neuropathological cohort study, 2004-2013. Participants resided in Chicago retirement communities and subsidized housing. The study included 286 autopsied brains of 554 deceased participants (51.6%). The mean (SD) age at death was 89.9 (6.1) years, 67% (193) were women, and the mean (SD) educational attainment was 14.6 (2.7) years.
EXPOSURES:Seafood intake was first measured by a food frequency questionnaire at a mean of 4.5 years before death.
MAIN OUTCOMES AND MEASURES:Dementia-related pathologies assessed were Alzheimer disease, Lewy bodies, and the number of macroinfarcts and microinfarcts. Dietary consumption of seafood and n-3 fatty acids was annually assessed by a food frequency questionnaire in the years before death. Tissue concentrations of mercury and selenium were measured using instrumental neutron activation analyses.RESULTS:Among the 286 autopsied brains of 544 participants, brain mercury levels were positively correlated with the number of seafood meals consumed per week (ρ = 0.16; P = .02). In models adjusted for age, sex, education, and total energy intake, seafood consumption (≥ 1 meal[s]/week) was significantly correlated with less Alzheimer disease pathology including lower density of neuritic plaques (β = -0.69 score units [95% CI, -1.34 to -0.04]), less severe and widespread neurofibrillary tangles (β = -0.77 score units [95% CI, -1.52 to -0.02]), and lower neuropathologically defined Alzheimer disease (β = -0.53 score units [95% CI, -0.96 to -0.10]) but only among apolipoprotein E (APOE ε4) carriers. Higher intake levels of α-linolenic acid (18:3 n-3) were correlated with lower odds of cerebral macroinfarctions (odds ratio for tertiles 3 vs 1, 0.51 [95% CI, 0.27 to 0.94]). Fish oil supplementation had no statistically significant correlation with any neuropathologic marker. Higher brain concentrations of mercury were not significantly correlated with increased levels of brain neuropathology.
CONCLUSIONS AND RELEVANCE:In cross-sectional analyses, moderate seafood consumption was correlated with lesser Alzheimer disease neuropathology. Although seafood consumption was also correlated with higher brain levels of mercury, these levels were not correlated with brain neuropathology.
The mainstream news outlets in the U.S. tell us we are in the midst of a narcotic use epidemic. People are dropping like flies from overdose.
Narcotics are also called opioids. I’m talking about oxycodone, hydrocodone, hydromorphone (Dilaudid), morphine, fentanyl, heroin, etc. Not Xanax, Ativan, or Valium.
On average, it takes three weeks of daily narcotic use to get physically dependent on it. “Dependent” means that when you stop the drug completely and suddenly, your body may crave it and you could have withdrawal symptoms. The severity of withdrawal symptoms varies from person to person. Possible symptoms include anxiety, sweating, nausea, vomiting, diarrhea, hyperactivity, restless legs, weakness, easy fatigue, shaking, suicidal thoughts, insomnia, and muscle pain or cramps.
Good and bad news, bad news first: Narcotic withdrawal can be very uncomfortable but rarely causes medically serious complications. The serious complications are usually in folks with pre-existing heart disease, high blood pressure, low blood pressure, or heart rhythm disturbances.
Here’s how you stop your chronic daily narcotic habit without suffering a withdrawal syndrome (if needed, see the postscript for an example):
- Total up your current total daily dose in milligrams
- Determine 10% of the amount by dividing the milligrams by 10
- Reduce your daily milligram intake by that 10% every week
- Nine weeks later you’ll be off narcotics
Congratulations! You’ve done your part to solve America’s opioid crisis. You’ve reduced your drug bill, avoided Opiate Use Disorder, and reduced your risk of narcotic overdose death by 100%. And you did it without political meddling or an expensive stay at a detox center.
Be aware that as you taper off your narcotic, you may have a flare of an underlying psychiatric condition such as depression, anxiety, PTSD, bipolar disorder, panic attacks, or psychosis. If so, see a mental health professional posthaste.
Good luck, America!
PS: Take Percocet 10/325 for example. It’s 10 mg of oxycodone and 325 mg of acetaminophen. Say you’re taking Percocet 10/325, four pills at at time, four times a day. That’s a total daily oxydocodone dose of 160 mg (16 pills x 10 mg). 160 mg divided by 10 = 16 mg. We have to round off 16 mg to 15 mg due to the availability of various strengths of Percocet. So starting today, you reduce your daily oxycontin dose by 15 g, which is one-and-a-half pills. After one week, you reduce your daily pill count by another one-and-a-half pills. Etc.
PPS: Let you’re doctor know what you’re doing beforehand. He’ll be overjoyed and ensure it’s safe for you to do this taper.
Gary Taubes argues that sugar is the likely cause of the Western world’s epidemics of obesity, type 2 diabetes, had heart disease.
I agree it’s a strong contributor to those maladies, if only via it’s contribution to overweight and obesity. I wouldn’t say it’s the sole cause.
Here’s an excerpt from Guyenet’s response to Taubes to whet your appetite:
A Slow-Acting Toxin
According to Taubes, sugar may be a “toxin” and “the primary cause of diabetes, independent of its calories, and perhaps of obesity as well.” Elsewhere in the essay, coronary heart disease is added to the list. Yet Taubes asserts that this speculative hypothesis cannot currently be tested because there is so little existing research on sugar, and so little interest in conducting such research, that the research necessary to nail it down would take years to decades to complete and is not even on the radar screen of the funding agencies.
This belief is remarkable in light of the fact that a Google Scholar search returns hundreds of scientific papers on the health impacts of sugar, many of them human randomized controlled trials, and many funded by the U.S. National Institutes of Health. In reality, the health impacts of sugar are of considerable interest to the scientific community, and as such, they have been studied extensively. Having established that this research exists, let’s take a look at it.
The hypothesis that sugar is the primary cause of coronary heart disease is easily refuted. In the United States, coronary heart disease mortality has plummeted by more than 60 percent over the last half century, despite a 16 percent increase in added sugar intake. Roughly half of this decline can be attributed to better medical care, while the other half is attributed to underlying drivers of disease such as lower cholesterol and blood pressure levels and an impressive drop in cigarette use. This striking inverse relationship is incompatible with the hypothesis that sugar is the primary cause of coronary heart disease, although it doesn’t exonerate sugar.
Is sugar the primary cause of diabetes, “independent of its calories”? Research suggests that a high intake of refined sugar may increase diabetes risk, in large part via its ability to increase calorie intake and body fatness, but it is unlikely to be the primary cause. An immense amount of research, including several large multi-year randomized controlled trials, demonstrates beyond reasonable doubt that the primary causes of common (type 2) diabetes are excess body fat, insufficient physical activity, and genetic susceptibility factors.
The ultimate test of the hypothesis that sugar is the primary cause of obesity and diabetes would be to recruit a large number of people—perhaps even an entire country—and cut their sugar intake for a long time, ideally more than a decade. If the hypothesis is correct, rates of obesity and diabetes should start to decline, or at the very least stop increasing. Yet this experiment is far too ambitious to conduct.
Or is it? In fact, this experiment has already been conducted—in our very own country. Between 1999 and 2013, intake of added sugar declined by 18 percent, taking us back to our 1987 level of intake. Total carbohydrate intake declined as well. Over that same period of time, the prevalence of adult obesity surged from 31 percent to 38 percent, and the prevalence of diabetes also increased.
Enjoy the view:
In stopping an epidemic, nothing is more important than correctly identifying its cause. Where we are today with obesity and diabetes reminds me of where infectious disease specialists were through most of the 19th century, when they blamed malaria and other insect-born diseases on miasma, or the bad air that came out of swamps. That was mildly effective, in that it was an explanation for why the rich in any particular town preferred to build their homes on hills, high above the miasma and, incidentally, away from the swamps and lowlands and slums where the vectors of these diseases were breeding. But only by identifying the vectors and the actual disease agents do we help everyone avoid them and eradicate the diseases. Only by unambiguously identifying the cause can we effectively design treatments to cure it. The kinds of explanations that Dr. Guyenet and Freedhoff put forth – highly palatable foods or ultra-processed foods – are the nutritional equivalents of the miasma explanation. They sound good; they might help some people incidentally eat the correct diets or offer a description of why other people already do, but they’re not the proximate cause of these epidemics. And there is a proximate cause. We have to find it. I can guarantee it’s not saturated fat, regardless of the effect of that nutrient on heart disease risk. What is it?
Now I am going to focus primarily on Dr. Guyenet’s response, as his was by far the most antagonistic, questioning both the history I present in the lead essay as well as the conclusions I’ve derived from the history and the science. While Dr. Guyenet does indeed challenge “specific and testable assertions” related to my lead essay, the one assertion he does manage to refute successfully is not, regrettably, an assertion I made in the article. As for the rest, the evidence against is not nearly as compelling as he presents it.
First, Dr. Guyenet examined “the 1980 Dietary Guidelines to determine if they condemn fat and take a weak stance on sugar as suggested.” He then set out to determine whether the 1980 Guidelines contributed to obesity, diabetes, and coronary heart disease. He concluded that they didn’t.
I was under the impression when I wrote the essay, though, and still am upon re-reading it, that I do not make such a simplistic assertion. The point that I made is not about the 1980 USDA Guidelines alone – Dr. Guyenet and I both note that they urged readers to avoid too much sugar – but rather the entire movement of the research community to demonize fat, and the journalistic coverage of it, and the series of government documents, and the consensus conferences that followed along because of it—all part of the same concerted public health effort that led us by the late 1980s to believe that the essence of a healthy diet is its relative absence of fat and saturated fat. As an unintended consequence, this ill-conceived dogma-building directed attention away from the possibility that sugar has deleterious effects independent of its calories.
These government reports, as I noted, included the FDA GRAS report on sugar in 1986, the Surgeon General’s Report on Nutrition and Health in 1988, the National Academy of Sciences Diet and Health report in 1989, the British COMA report on food policy the same year, and others. I could have also mentioned the 1984 NIH consensus conference on “lowering blood cholesterol to prevent heart disease” that followed on this legendary Time Magazine cover – “Cholesterol, And Now the Bad News” – and the founding in 1986 of the National Cholesterol Education Program, which published its guidelines for cholesterol lowering the following year. All focused on dietary fat and serum cholesterol as the agents of heart disease and all mostly or completely ignored the evolving science on insulin resistance and metabolic syndrome that implicated sugar and other processed carbohydrates.
Indeed, if anything, the more relevant of the two USDA Dietary Guidelines, the one that Dr. Guyenet does not address, is the 1985 version that declared without a caveat, as I noted, that “too much sugar in your diet does not cause diabetes.” This is, of course, remains the critical question and the one that yet has to be rigorously tested (ignoring the tautology implied by the use of the words “too much”).
Dr. Guyenet, Dr. Freedhoff, and I all agree that had Americans eaten as the guidelines cautioned (and just as Michael Pollan would have preferred as well), we’d all very likely be healthier. But we didn’t. The question is whether the dietary fat/serum cholesterol/heart disease obsession directed attention away from the hypothesis that sugar causes heart disease, diabetes, and perhaps obesity as well through its effect on insulin resistance. The secondary question is whether this obsession in government documents, programs, journalistic coverage, and (pseudo)scientific reviews explains why we continued to eat such high sugar diets. As Dr. Guyenet notes, Americans still consume a significant amount of our calories from grain-based desserts and sugary beverages. But why? By focusing on the straw man of the 1980 guidelines, Dr. Guyenet fails to address that question. That he’s taking on a straw man makes me thinks he’s more interested in appearing to win an argument than in dealing with what may be the single most important public health issue of our era.
A key point to make, as Professor Kealey does, is that Americans did indeed respond to the dietary dogma of the 1970s and 1980s by changing their diets. Dr. Freedhoff and Dr. Guyenet are wrong in this regard when they attend only to the total percentage and amounts of fats, carbohydrates, and protein in our diets, and not the type of fats, carbohydrates, and even protein. Looking at what we ate instead of how much we ate supports the supposition that Americans heard the advice on fat and acted on it, even as we were ignoring the sugar advice. As the USDA reports, between 1970 and 2005, we cut down on our use of butter (-17%) and lard (-66%), while almost doubling vegetable oil consumption (from 38.5 pounds per capita yearly to 73.7); we more than doubled how much chicken we ate (33.8 pounds per capita yearly to 73.6, probably skinless white meat, but I’m speculating), while reducing our red meat consumption by 17 percent, and beef by 22 percent. We cut back on eggs, too. So while total fat consumption decreased only marginally, as Drs. Freedhoff and Guyenet note, that marginal decrease is accompanied by a reduction in animal fats and their replacement by vegetable oils, which were thought to be heart healthy and still are (perhaps also erroneously). The type of fats we consumed and the type of foods we consumed changed significantly, and this change was very much in accord with what we were being told.
The post-1980 focus on dietary fat also led to the creation and sale of thousands, perhaps tens of thousands, of non-fat and low-fat food-like substances (credit for the terminology once again to Mr. Pollan). In this instance, the CDC’s publication Healthy People 2000 is informative: Healthy People 2000 included multiple “nutrition objectives” aimed at reducing dietary fat consumption, including the creation of 5,000 low-fat or low-saturated fat products. It included nutrition objectives to reduce salt intake and increase complex carbohydrate and fiber consumption, but included no such objective for sugar or sugar-rich foods. Why not? Indeed, I find that the words “sugar” or “sugars” appear only five times in the almost 400-page final review of how well the guidelines were met. In 1995, the American Heart Association counseled in one of its pamphlets that Americans could control the amount and kind of fat consumed by “choos[ing] snacks from other food groups such as…..low-fat cookies, low-fat crackers,…unsalted pretzels, hard candy, gum drops, sugar, syrup, honey, jam, jelly, marmalade (as spreads).” In 2000, the AHA published this cookbook of low-fat and luscious sugar-rich “soul-satisfying” desserts. I don’t know if Dr. Guyenet would describe this as a “weak stand” on sugar or not, but it does shed light on our failure to limit sugar consumption during a period in which all public health advice was focused on reducing fat.
The more important question, and a very different one, is whether our sugar consumption has uniquely deleterious effects on our health. To refute the claim that consuming sugar might cause heart disease, Dr. Guyenet points out that heart disease mortality has dropped precipitously over the years of the obesity and diabetes epidemics and during a period when sugar consumption clearly increased (technically “caloric sweeteners” since the increase was due primarily to high-fructose corn syrup). Professor Kealey makes a similar point but with a far more nuanced perspective about how mortality rates are confounded by what are, after all, a half-century’s worth of very concerted efforts by medical researchers, the pharmaceutical and medical industry, and public health authorities to reduce mortality. That these efforts succeeded in reducing mortality is indeed commendable, but it makes it far more difficult than Dr. Guyenet suggests to derive meaning from the mortality data. If it’s evidence against the sugar hypothesis, it’s very weak evidence.
DiaTribe has an article on glucose meter accuracy by Jeemin Kwon and Adam Brown. I quote:
Results from the Diabetes Technology Society’s Blood Glucose Meter Surveillance Program identifies only six out of 18 meters that passed. Did yours make the cut?
The Diabetes Technology Society (DTS) recently revealed long-awaited results from its Blood Glucose Monitor System (BGMS) Surveillance Program. The rigorous study tested the accuracy of 18 popular blood glucose meters (BGM) used in the US. These FDA-cleared meters were purchased through retail outlets and tested rigorously at three study sites in over 1,000 people (including 840 people with diabetes). The results were troubling: only six out of the 18 devices met the DTS passing standard for meter accuracy – within 15% or 15 mg/dl of the laboratory value in over 95% of trials.
The devices that passed were:
- Contour Next from Ascensia (formerly Bayer) – 100%
- Accu-Chek Aviva Plus from Roche – 98%
- Walmart ReliOn Confirm (Micro) from Arkray – 97%
- CVS Advanced from Agamatrix – 97%
- FreeStyle Lite from Abbott – 96%
- Accu-Chek SmartView from Roche – 95%
The devices that failed were:
- Walmart ReliOn Prime from Arkray – 92%
- OneTouch Verio from LifeScan – 92%
- Prodigy Auto Code from Prodigy – 90%
- OneTouch Ultra 2 from LifeScan – 90%
- Walmart ReliOn Ultima from Abbott – 89%
- Contour Classic from Bayer – 89%
- Embrace from Omnis Health – 88%
- True Result from HDI/Nipro – 88%
- True Track from HDI/Nipro – 81%
- Solus V2 from BioSense Medical – 76%
- Advocate Redi-Code+ from Diabetic Supply of Suncoast – 76%
- Gmate Smart from Philosys – 71%
Drugs to control hypertension can save your life. I prescribe them all the time. However, there are also “natural” ways to control high blood pressure. Click the link at bottom for some of the better known methods from Kerri-Ann Jennings, RD. If you’re trying to avoid drugs, you’ll probably need a combination of tricks. And they don’t work for everybody.
Even if you’re already on drugs, you may be able to cut back or stop them if you adopt some of these tips.
“High blood pressure is a dangerous condition that can damage your heart. It affects one in three people in the US and 1 billion people worldwide.
If left uncontrolled, it raises your risk of heart disease and stroke.
But there’s good news. There are a number of things you can do to lower your blood pressure naturally, even without medication.Here are 15 natural ways to combat high blood pressure.”
h/t Jan at The Low Carb Diabetic
The U.S. Food and Drug Administration has issued new guidelines for manufacturers of home glucose monitoring devices. The old standard was that the glucose reading of the device had to be within 20% of the actual or true value compared to a medical lab-grade machine.
For example, if the device read 165 mg/dl, the true value could be anywhere from 132 to 198 mg/dl. Or if you think in mmol/l terms, a reading of 9.2 could be anywhere from 7.3 to 11.
Under the new +/- 15% rule, the true number should be between 140 and 190 mg/dl.
I bet you thought your device was more accurate than that.
“Blood glucose test results are used by people with diabetes to make critical decisionsabout their treatment; therefore, it is important that the results are accurate so that nutritional and drug dosing errors are better avoided. Your studies should demonstrate that your SMBG is sufficient for this purpose by showing that 95% of all SMBG results in this study are within +/- 15% of the comparator results across the entire claimed measuring range of the device and that 99% of all SMBG results are within +/- 20% of the comparator results across the entire claimed measuring range of the device.”
I need to reach more people. Last fall I tripled my blogging frequency and it did nothing to increase viewership. I plan to cut back on written blogging and Tweeting, but will be doing more videos. It’s an experiment.
I’ll try to keep all videos under six minutes out of respect for your time.
This video mentions the topics I’ll be covering. If they sound interesting, please subscribe to the pxHealth YouTube Channel.
Even if you have T2 diabetes already, share this post with someone who has prediabetes or risk of getting diabetes. You could save a life and prevent a lot of hassle.
“A new study, published this week in the journal Diabetologia, takes a deeper look at the role of exercise in the development of type 2 diabetes. It is the most in-depth study to examine exercise independent from other influential factors, such as diet. The conclusions from the report are clear: “This research shows that some physical activity is good, but more is better.” (says study co-author Dr. Soren Brage)
Currently, physical activity guidelines in the U.S. and the United Kingdom recommend 150 minutes of moderate activity or 75 minutes of vigorous activity per week; this could include cycling, walking, or sports. However, according to the Centers for Disease Control and Prevention (CDC), fewer than 50 percent of American adults meet these recommendations.
The current study was a result of collaborative work between two institutions – University College London and the University of Cambridge, both of which are based in the U.K. Data from more than 1 million people was collated. In all, the team analyzed 23 studies from the U.S., Asia, Australia, and Europe.”
“According to the analysis, cycling or walking briskly for 150 minutes each week cuts the risk of developing type 2 diabetes by up to 26 percent.
Those who exercise moderately or vigorously for an hour each day reduced their risk by 40 percent. At the other end of the scale, for those who did not manage to reach the 150 minute target, any amount of physical activity they carried out still reduced the risk of type 2 diabetes, but to a lesser extent.”
Steve Parker, M.D.
PS: If you want to start an exercise program, my books will get you started.
Many folks find it difficult to drink the usual recommended eight 8-oz glasses of water daily. That makes me wonder if there’s an underlying evolutionary mechanism at play, and maybe we don’t need that much water. Drinking untreated water exposes us to disease-causing organisms. The more water, the more pathogens.
I quote MNT:
“But how much water do we need to drink on a daily basis?
While you may have heard that eight 8-ounce glasses of water each day – known as the “8×8 rule” – is the aim, there is no scientific evidence that pinpoints precisely how much fluid is the optimal amount.
Based on studies to date, the Institute of Medicine (IOM) recommend that women should aim to drink around 2.2 liters of total beverages daily (around 9 cups), while men should aim to consume around 3 liters of total beverages daily (around 13 cups).
However, contrary to these recommendations and the so-called 8×8 rule, the new study suggests we should only drink when we are thirsty, after discovering a mechanism that makes drinking excess water challenging.”