Fats & Sperm This one is going to be little different. The main topic will be the truth about fats and their effect on sperm count. The sub-plot will be the huge game of propaganda on this story. I was shocked as began to research my hypothesis that a low fat diet would reduce sperm count, since cholesterol is required for testosterone and spermatozoa to develop. The shock was when my Google search came back with the same headline over and over for several pages of results. For fun search "low sperm count and fatty acids" and see what you get. (or click the link) OMG! Fatty foods REDUCE sperm count? Drats! My hypothesis up in flames before I even start? OK, well the scientific method encourages this, try to disprove your theory, OK, I'm in. Let's look at the actual study here. It was done in a pretty sloppy way, too many variables, some were significant. It was an observational study of only 99 men, the study depended on a questionnaire asking men to state what their diet consisted of. It is well known that retrospective questionnaires are very inaccurate for rigorous tests. They tested 23 of the 99 men semen and blood, but not all 99. 71% of the men were obese or overweight. This is very significant. Let's talk about what that has to do with sperm count. "Obese people have larger and more abundant adipocytes (the cells that form adipose tissue), adipocytes are loaded with an enzyme known as aromatase which is the chief culprit in the transformation of testosterone into estrogen." The Medicine Daily blog points out; thankfully someone who is doing due diligence on a study like this. "Estrogen is involved in a negative feedback loop with the hypothalamus – when the hypothalamus detects high levels of estrogen it slows down testosterone production by limiting LH and FSH (Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) are called gonadotropins) from the pituitary gland. The chain is known as the HPGA (hypothalamus-pituitary-gonadal axis) or HPTA (hypothalamus-pituitary-testicular axis). When LH and FSH (primarily FSH) levels fall, sperm production begins to decline – this is why men become less fertile as they age and why men on testosterone replacement therapy have a difficult time conceiving – due to diminished FSH levels. Now, if those men were already obese it is likely that they already have a lower sperm count due to high circulating estrogen and lower FSH. When fed a diet of saturated fats (which has been shown to increase testosterone, here and in other instances, as steroid hormones are derived from lipids) their estrogen levels are likely to rise even more due to conversion of testosterone to estrogen. This will further lower FSH levels." To be fair, the Dr. who did the study has excellent credentials: Prof Jill Attaman is currently Assistant Professor of Obstetrics and Gynecology at Dartmouth Medical School and a Reproductive Endocrinology and Infertility Subspecialist at Dartmouth-Hitchcock Medical Center. She did state more than once in here findings that they were inconclusive and needed more clinical research. "Given the limitations of the current study, in particular the fact that it is a cross-sectional analysis and that it is the first report of a relation between dietary fat and semen quality, it is essential that these findings be reproduced in future work." however this caveat ends here. She made several statements indicating her bias and made her suggestions known which the press just gobbled up and sprayed all over the headlines with scary pictures of fatty foods. (See above) Of note: 71% of all the men in the study were overweight or obese, and the health effects of this could also affect semen quality. However, the researchers made allowances for this. "We were able to isolate the independent effects of fat intake from those of obesity using statistical models," said Prof Attaman. "Notably, the frequency of overweight and obesity among men in this study does not differ much from that among men in the general population in the USA (74%)." So they were saying that they used some fancy math to determine everything that might also have caused the reduction is healthy semen? If you can do that, then you could solve the issue straight away, right?
She went on to say the big agenda item here: "In the meantime, if men make changes to their diets so as to reduce the amount of saturated fat they eat and increase their omega-3 intake, then this may not only improve their general health, but could improve their reproductive health too. At a global level, adopting these lifestyle modifications may improve general health, as high saturated fat diets are known to be a risk factor for a range of cardiovascular diseases; but, in addition, our research suggests that it could be beneficial for reproductive health worldwide." OK, so we're done with this study, take it with a grain of salt. Omega-3's can really help reproductive health This study is really on to something. If you've read my post on Fat you'll see much more on the Omega-6/Omega-3 ratio and it's effects on your overall health. It's entitled "Relationship of omega-3 and omega-6 fatty acids with semen characteristics, and anti-oxidant status of seminal plasma: a comparison between fertile and infertile men." Methods: "Eighty-two infertile men with idiopathic OAT and seventy-eight fertile men defined according to semen concentration and proven fertility were enrolled in the study. The semen parameters were assessed according to World Health Organization criteria; three omega-3 fatty acids--alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and two omega-6 fatty acids--linoleic acid (LA) and arachidonic acid (AA) concentrations were measured in blood plasma and spermatozoa; and the seminal plasma enzymatic antioxidant levels of catalase, and superoxide dismutase (SOD) were also assessed." Now that looks like a clinical study, two groups of nearly equal size and a single determining factor was studied by playing around with a few variables. Conclusions: "Infertile men had lower concentrations of omega-3 FAs in spermatozoa than fertile men. These results suggest that research should be performed to assess the potential benefits of omega-3 FA supplementation as a therapeutic approach in infertile men with idiopathic OAT." You can read the results, which are pretty technical in nature, but their conclusion did not make too much of a splash because it did not go along with the "fats are bad" agenda. Another clinical study "An omega-3 fatty acid, docosahexaenoic acid (DHA), is enriched in testicular membrane phospholipids, but its function is not well understood. The Fads2 gene encodes an enzyme required for the endogenous synthesis of DHA. Using Fads2-null mice (Fads2/), we found in our preceding studies that DHA deficiency caused the arrest of spermiogenesis and male infertility, both of which were reversed by dietary DHA." Look on the back of your fish-oil and see how much DHA is available. Ours is made by Nordic Naturals, it has 550 mg of DHA and 825 mg of EPA. Conclusion: If you eat junk food it's bad for you in many ways, stop doing that. Beyond that, Omega-6 will reduce your ability to produce healthy sperm when out of balance with Omega-3's. More Omega-3's will increase productivity of healthy swimmers. Eating saturated fats from healthy natural sources will not hamper your ability to reproduce, but being obese will. I hope that helps clear things up.
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Dementia & Alzheimers A great article on Yahoo states: Although Alzheimer's is now one of the most common diseases of the elderly, the condition barely existed before 1960. "I looked everywhere. I looked on three continents and in every medical library I could find, including the Library of Congress and the British Museum library," said Alzheimer's specialist Murray Waldman, MD, from St. John's Rehabilitation Hospital in Toronto, Canada. "No matter where I looked, I couldn't find anything that indicated there was very much Alzheimer's prior to the 1960s." Epidemiological data collected over a 25-year period shows the incidence of Alzheimer's in the 1960s was 2% in people over the age of 85 years. Today, it's incidence in this population is 50% or more. It's incidence in people over 75 is 20% - and 10% in individuals over the age of 65. Between 1996 and 2000 the incidence of Alzheimer's and other dementias shot up from 1274 to a stunning 21,569 during the same time period. "This dramatic spike over 40 or so years, he said, cannot be accounted for by an aging population, because what we were looking at was incidence, not prevalence," Dr. Waldman points out. In another study I found on WebMD.com, there was a link to dementia and low HDL. Although poor memory in middle age has not been directly linked to Alzheimer's disease and other forms of dementia in old age, memory decline is key to the diagnosis of these conditions, lead researcher Archana Singh-Manoux, PhD, tells WebMD. "Our research does not show a link between HDL and dementia," she says. "We looked at cognitive decline in midlife, but it may turn out that this decline is a risk factor for dementia." Researchers have attempted to study HDL and other lipids like low-density lipoprotein (LDL), total cholesterol, and triglycerides in patients with Alzheimer's and other age-related dementias, but these studies have proven problematic, Singh-Manoux says. "By the time people are diagnosed they have usually had the disease for many years, and the disease itself may have modified these lipid profiles," she says. Type 3 Diabetes (yes there is a type 3) In this research, Alzheimer's Disease Is Type 3 Diabetes–Evidence Reviewed "Even before the initial study had been published, it was realized that if brain insulin/IGF (Insulin-like Growth Factor) resistance and insulin/IGF deficiency were causal in the pathogenesis of Alzheimer's Disease (AD), the related abnormalities should be detectable in the early stages of disease and possibly worsen as disease progresses." "Altogether, the results from these studies provide strong evidence in support of the hypothesis that AD represents a form of diabetes mellitus that selectively afflicts the brain. Positive data stemmed from (3) direct analysis of postmortem human brains with documented AD; (4) an experimental animal model in which brain diabetes with cognitive impairment and molecular and pathological features that mimic AD was produced by intracerebral administration of a drug that is commonly used to produce Type 2 Diabetes Mellitus (TDM) and (5) a study showing that PPAR (peroxisome proliferator-activated receptors) T1DM (Type 1 Diabetes Mellitus) or T2DM; and (5) a study showing that PPAR agonists, which are used to treat T2DM, prevent many of the AD-associated neurodegenerative effects of ic-STZ. (Which is basically the clinical word for Type-3 Diabetes) The data are supported by abundant in vitro experiments that demonstrated essentially the same or similar effects of STZ or oxidative stress treatments of neuronal cells." A study on rats by experts from Brown University suggest that a similar process could affect the brain, which relies on insulin to regulate nerve signals related to memory and learning and to produce energy from glucose. Researchers found that blocking insulin from rats' brains made them disoriented and unable to find their way out of a maze because they could not remember where they were. Examination of their brains showed the same pattern of deterioration seen in Alzheimer's patients, including increased levels of the amyloid plaque which is a key hallmark of the condition. Conclusion So, what they are basically stating is that in clinical trials, there were able to isolate the cause and reverse some of the effects of Alzheimer's Disease if viewed as a form of insulin resistance. Since the brain primarily runs on glucose as a fuel source, the brain is primarily made of fats, insulin resistance could be very problematic for brain tissues. "Altogether, the data provide strong evidence that AD is intrinsically a neuroendocrine disease caused by selective impairments in insulin and IGF signaling mechanisms, including deficiencies in local insulin and IGF production." However, if you are not running on the glucose fuel system by being in nutritional-ketosis, you can prevent and reverse the destructive effects of sugar on the brain. 3. Jalbert JJ, Daiello LA, Lapane KL. Dementia of the Alzheimer Type. Epidemiol Rev. 2008. [Epub ahead of print.]
4. Jellinger KA. Neuropathological aspects of Alzheimer disease, Parkinson disease and frontotemporal dementia. Neurodegener Dis. 2008;5(3-4):118–21. 5. Wang XP, Ding HL. Alzheimer’s disease: epidemiology, genetics, and beyond. Neurosci Bull. 2008;24(2):105–9. Why are we dealing with so many illnesses? Why are people losing their gallbladders in their forties? Why is dementia and alzheimer's on the rise? What about the dramatic decrease in sperm count? How come so many people have vitamin D deficiency? With all of our technology, mapping the human genome and all, huge sums of money for research -- where are the answers? We'll be doing at least a four-part series on these topics. For more than the past 50 years, we've been told that we need to reduce our fats. Even today's American Heart Association continues this mantra: Limit foods and beverages high in calories but low in nutrients, and limit how much saturated fat, trans fat, cholesterol and sodium. Read labels carefully — the Nutrition Facts panel will tell you how much of those nutrients each food or beverage contains. So, since we seem to always question the status quo, (because it's not working) let's look into this from the position of evidence and facts. Perhaps we'll discover the answers together. Gallbladders First you need a little Anatomy-Physiology 101 I mentioned in my WHY the challenges of being a teacher with all the constant goodies that are always left for anyone in the break room. I am a high school Chemistry, Biology and Anatomy Teacher. This write up will feature the scoop on the way our livers and gallbladders interact with the foods we eat, in a simple and generalized way so it is easy to understand the basics. Our livers are responsible for cleaning toxins out of our blood, making cholesterol (or transforming it into different types), getting rid of bilirubin (the remains of dead red blood cells), and supporting digestive processes. Toxins are released from the blood into the liver and end up in the bile ducts that feed into the gallbladder as the toxins drain from the ducts. Not every toxin travels this way, but many metabolic toxins do. When the day is done, up to 1,500 mL of bile has been produced. If the small intestines are empty, the gallbladder is in storage mode, holding all the bile to be released once food comes along. When food comes through the intestine, the duct will open from the gallbladder and bile will begin to drain. However, when fats or proteins come through the intestine it signals the release of cholecystokinin (CCK). This hormone causes the gallbladder to contract and empty its contents into the small intestine and stimulates the release of pancreatic juices to also be released. The more times the gallbladder empties, the more bile will flow out of the gallbladder and out of the liver. When the gallbladder doesn’t contract regularly the bile salts irritate the lining of the gallbladder so that the bladder produces mucus that causes a thickening of the bile contents. Continued storage of this substance causes the formation of stones -- gallstones. Since toxins are released from the body through the liver/bile processes, it stands to be smart to make sure the gallbladder receives the signal for full release of the gallbladder contents frequently to keep the liver and gallbladder clean. America has been experiencing epidemic levels of gallstones followed by gallbladder removal surgeries. Another issue of note is the frequency needed for the cleansing of the liver using herbal remedies, that is being touted by the alternative health community for the past 15-20 years. It is interesting to consider the drop in the consumption of animal fats and the rise of liver and gall bladder issues; could there be a connection? I realize that many reading this may no longer have their gallbladders, but the gall is still flowing from your liver. You should still be able to enjoy living on this food plan if you space out your fat consumption and figure out your rhythm of when your body does better with the fat, as in finding when your body is releasing more bile. I am aware of the pain and discomfort that can come from the lack of bile. Choosing which fats is also key. In conclusion, keeping your liver clean and your gallbladder healthy takes fats, lots of fats and good protein. If you are interested in cleansing your liver, even if you have had your gallbladder out, here’s a terrific resource that has proven effective for us and family members that have used it. The Liver and GallBladder Miracle Cleanse by Andreas Moritz, Ulysses Press, 2007 Cheers to a healthy liver! Lynette On the Atkins site, this article addresses things directly and is well cited: "In recent years surgeons have been increasingly removing gallbladders, presumably in an attempt to treat gallstones and related disorders. But the gallbladder is fundamental to your well-being. Among other functions, it stores bile, a powerful fat-emulsifying substance that the liver makes from cholesterol. A healthy gallbladder works with flawless precision, releasing bile just when it’s needed to help digest food. It also absorbs nutrients and keeps your cholesterol levels in check. Even as many doctors subscribe to the myth that eating fat and cholesterol leads to gallstones, research indicates that eating too little fat and too many carbohydrates in the form of grains, sugars and starches actually leads to gallbladder ailments."(1) One study did discover that low fat, high carb diets caused more gallstones than expected. "Conclusions: Our findings suggest that a high intake of carbohydrate, glycaemic load, and glycaemic index increases the risk of symptomatic gallstone disease in men. These results add to the concern that low fat high carbohydrate diets may not be an optimal dietary recommendation." Another study stated even more clearly: "In the obese during rapid weight loss from a very low calorie diet, a relatively high fat intake could prevent gallstone formation, probably by maintaining an adequate gallbladder emptying, which could counterbalance lithogenic mechanisms acting during weight loss." There were several studies that discussed the side-effect of gastric banding and the dramatic weight loss actually caused gallstones to develop in obese subjects. Dietary fat and cholesterol promote normal gallbladder function.(2) If you take cholesterol-lowering drugs, be aware that they can raise the risk of gallstone formation. Conclusion Consuming sufficient healthy fat (saturated & monounsaturated) while shunning sugar and other carbohydrates promotes gallbladder contractions and prevents gallstones better than anything else. So, long before surgery becomes a necessity, look at changing your diet. It’s a lot safer. For those of you who have lost your gallbladder, you can still eat a low carb/high fat diet. Footnotes
1. Tseng, M., Everhart, J.E., Sandler, R.S., "Dietary Intake and Gallbladder Disease: A Review," Public Health Nutrition, 2(2), 1999, pages 161-172. 2. Gebhard, R.L., Prigge, W.F., Ansel, H.J., et al., "The Role of Gallbladder Emptying in Gallstone Formation During Diet-Induced Rapid Weight Loss," Hepatology, 24(3), 1996, pages 544-548.3. Michielsen P.P., Fierens, H., Van Maercke, Y.M., "Drug-Induced Gallbladder Disease. Incidence, Aetiology and Management," Drug Safety, 7(1), 1992, pages 32-45. So if you've read my story, you know that I eat a lot of fat. 70-75% of my 2000 calories per day diet comes from fat. When I say that, most people say, "good fats, right?" I say, "Yeah good like bacon fat, saturated fat, coconut oils." Most people make a classic 'disgust' face when I say saturated fats. When I say organic & grass-fed, they seem to warm up to the idea. Then they are very confused that eating fats could be good for them. Eating this way has reduced my triglycerides, increased my HDL and reduced my blood pressure. If this experiment of N=1 were the only one it would be interesting, but there are so many with similar stories. In fact it seems that is the way it works, you reduce your carbs, replace those calories with fats and your body springs back into health. It is a complex balance of Omega 3/6 fats that reduces inflammation and turns you into a fat-burning machine that gives you the results. But as you can see, you'll be swimming upstream if you try this lifestyle. Like we've said, sugar is everywhere, so are inflammatory oils. So what happened to our diets in the past century that caused all this disease? We reduced our animal fats for sure, however we increased our vegetable oils. The problem with vegetable oils they are very high in Omega 6 fatty acids. Vegetable oil consumption rose dramatically between the beginning and end of the 20th century, and this had an entirely predictable effect on the ratio of omega-6 to omega-3 fats in the American diet. Between 1935 and 1939, the ratio of n-6 to n-3 fatty acids was reported to be 8.4:1. From 1935 to 1985, this ratio increased to 10.3:1 (a 23% increase). Other calculations put the ratio as high as 12.4:1 in 1985. Today, estimates of the ratio range from an average of 10:1 to 20:1, with a ratio as high as 25:1 in some individuals. In fact, Americans now get almost 20% of their calories from a single food source – soybean oil – with almost 9% of all calories from the omega-6 fat linoleic acid (LA) alone! (source)
According to the CDC, we have a very big problem on our hands. Diabetes is one of the fastest growing diseases in America. I believe 90% of the cases are preventable, so before you get offended at my ignorance, first a few facts from the CDC.
Among U.S. residents aged 65 years and older, 10.9 million, or 26.9%, had diabetes in 2010. • About 215,000 people younger than 20 years had diabetes (type 1 or type 2) in the United States in 2010. • About 1.9 million people aged 20 years or older were newly diagnosed with diabetes in 2010 in the United States. • In 2005–2008, based on fasting glucose or hemoglobin A1c levels, 35% of U.S. adults aged 20 years or older had prediabetes (50% of adults aged 65 years or older). Applying this percentage to the entire U.S. population in 2010 yields an estimated 79 million American adults aged 20 years or older with prediabetes. • Diabetes is the leading cause of kidney failure, nontraumatic lowerlimb amputations, and new cases of blindness among adults in the United States. • Diabetes is a major cause of heart disease and stroke. • Diabetes is the seventh leading cause of death in the United States. THE GLOBAL BURDEN 366 million people have diabetes in 2011; by 2030 this will have risen to 552 million The number of people with type 2 diabetes is increasing in every country 80% of people with diabetes live in low- and middle-income countries The greatest number of people with diabetes are between 40 to 59 years of age 183 million people (50%) with diabetes are undiagnosed Diabetes caused 4.6 million deaths in 2011 Diabetes caused at least USD 465 billion dollars in healthcare expenditures in 2011; 11% of total healthcare expenditures in adults (20-79 years) 78,000 children develop type 1 diabetes every year Read more... |
AuthorsTim & Lynette Jenné are learners first and foremost. We love to ask "why?" We question the status quo. We also love to research and find answers for ourselves. As parents of four adult children, we've learned a few things along the way that may be helpful to others. We love to live & eat clean, simple lives. Archives
July 2015
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