http://www.thekitchn.com/feedburnermain
With Memorial Day behind us, the season of the picnic has arrived. From now through Labor Day, most of us will at some point decide to pack up a meal in a hamper or a cooler, head out to a park or a beach or a forest, lay out a blanket, and enjoy our meal en plein air. What is it about picnics that makes perfectly mono-lingual people speak French? And why is it that picnics are so enduringly appealing?
http://www.thekitchn.com/feedburnermain
What better duo to illustrate the ease of simple-yet-sublime summer desserts than berries and cream? Here, sun-kissed raspberries are enveloped in whipped coconut milk in a modern twist on the traditional British fool. And despite its classification as a vegan dessert, it’s every bit as luxurious — and light — as its dairy-filled counterpart.
http://chriskresser.com/
Alzheimer’s disease (AD) is a crippling, chronic, and progressive neurodegenerative disease that is conventionally understood to be irreversible. It is characterized by memory loss, dementia, cognitive impairment, and the presence of amyloid plaques in the brain (1, 2). Approximately 5.1 million people over the age of 65 in the United States are diagnosed with AD, along with another 200,000 under age 65. This estimate is predicted to increase by 10 million in the next 35 years (3).
In addition to those diagnosed, this disease changes the lives of more than 15 million family members and caregivers. Today, the estimated annual out-of-pocket expense plus the value of the approximately 18.1 billion volunteer caregiver hours approaches a staggering $440 billion (4). Unless there are advances in the cause and treatment of AD by the year 2050, that number will approach $1 trillion. The Centers for Disease Control & Prevention reports that AD is the sixth leading cause of death in the United States (4, 5). James et al. (2014) suggest that AD-related deaths are underreported and estimate that it is actually the third leading cause of death after heart disease and cancer (6).
Alzheimer’s disease was first characterized and diagnosed over 100 years ago (7). Since that time, ideas on the pathology and treatment of AD have shifted from a focus on amyloid plaques in the brain as the cause (8), to misfolded tau proteins (9), to focus on the genetic heritability of the disease, to epigenetic influences (10, 11), to inflammation as a primary culprit (2), to medication-induced mitochondrial dysfunction (12), and to metabolically influenced mechanisms (13, 14, 15).
The breadth of Alzheimer’s research speaks to how elusive this disease really is. Despite the uncertainty of specific causal mechanisms, there are currently five prescription drugs that are used to combat the symptoms of AD. The last drug approved to treat the symptoms of Alzheimer’s disease was brought on the market in 2003. Over the decade spanning 2002 to 2012, there were 413 AD drug trials performed; nearly four out of five of those clinical trials were sponsored by pharmaceutical companies. Trials were designed to test cognitive improvement, particular disease-modifying small molecules, and immunotherapies. The overall success rate over that period of time was measured to be 0.4 percent (99.6 percent failure) (1).
Recently, a group of 33 Alzheimer’s researchers joined forces to raise awareness about a neglected piece of the Alzheimer’s puzzle: the correlation between the manifestation of this disease and the microbial world (16).
An infectious disease is one that is caused by a pathogenic microbe and may be spread directly or indirectly (17). Infectious disease rates have plummeted over the course of the past century due to advances in sanitation, vaccination, and treatment (18). Historically, once a disease is identified to be infectious in origin, treatment and prevention protocols have been successful.
The idea that Alzheimer’s disease may be an infectious disease is supported by a number of observations. There have been many correlations between common infectious and immune-challenging agents and the diagnosis of AD (16).
Could Alzheimer’s be an infectious disease? Some research says yes.
“Seeding” Alzheimer’s disease in mice. Researchers have successfully created senile plaques associated with AD by infusing dilute fluid from the neocortex of Alzheimer’s patients into mice (19). These results highlight a key pathogenesis for neurodegenerative disease in mice and open up avenues for research in human subjects.
Type 2 diabetes and Alzheimer’s disease. A link between type 2 diabetes and AD has been suggested as both diseases present with local inflammation and amyloidosis (misfolded proteins) and are both associated with the presence of a common microbial community that includes Chlamydophyla pneumoniae, Helicobacter pylori, and spirochetes (20).
Periodontitis and Alzheimer’s disease. There is a correlation between the diagnosis of AD and periodontitis (21). Researchers hypothesize that the microbes living in dental plaque biofilm invade the brain via the bloodstream or peripheral nerves and promote inflammation of the central nervous system, which is known to be associated with cognitive decline (21, 22, 23).
Herpes simplex virus 1 and Alzheimer’s disease. Herpes simplex virus type 1 (HSV1) is quite common in the general population; roughly 70 percent of people over the age of 50 have been exposed to it. HSV1 was first proposed to be associated with AD nearly 35 years ago (24). This hypothesis was made plausible when researchers discovered a technique to test for the HSV1 virus in the human brain (25). After adjusting for known risk factors (age, education, APOE status) Letenneur et al. (2008) discovered a significant correlation between patients with primary or reactivated HSV1 (as measured by immunoglobulin M) and AD diagnosis (26, 27).
Atherosclerosis and Alzheimer’s disease. Atherosclerosis has been compared to AD because both diseases present with inflammation; are associated with viral and bacterial infection, including HSV1 and Chlamydophila; and are characterized by plaque formation. Researchers hypothesize that both are caused by a chronic immune challenge (infection) that induces cholesterol 25-hydroxylase expression (plaque) to protect the body locally against infectious agents (28).
Biotoxins and Alzheimer’s disease. A connection has been made between biotoxin exposure and a distinctive type of AD that affects younger people that is characterized by some combination of stroke-like speech impairment, partial Gerstmann’s syndrome, impaired ability to read, inability to interpret visual information, or impaired motor skills. This AD-type is “cortical” (14) and has now been reported in the literature as “inhalational Alzheimer’s disease” (IAD), a manifestation of chronic inflammatory response syndrome (CIRS) resulting from biotoxin exposure (29, 30).
Given the vast physical, mental, emotional, and financial burden that Alzheimer’s disease places on us, there is a dire need to be proactive. If the pathogenesis of AD includes an overlooked infectious component, there are many things that you can do starting today to decrease your odds of “contracting” this neurodegenerative disease.
It is not inaccurate to say that “health” is the best way to fight infection, but more specifically, a thriving, functioning immune system and a mindful perspective (31). An immune system under constant stress will slowly and steadily begin to malfunction over time, making our bodies more permissible to strange and pathogenic ecosystems (32, 33).
The best way to support your immune system and overall health is to provide your body with the information that it needs to operate and to make sure that the information delivered is in fact received. The receipt of this information is influenced by your overall gut health (34). Once gut health is considered, the required information from your environment comes from:
An “infectious disease” does not only manifest as an acute sickness; it may also manifest from chronic, progressive, and cumulative insults to the immune system over time.
Although I believe that Alzheimer’s (as well as most other modern diseases) is multifactorial and has several causes, the recognition that Alzheimer’s disease may be the result of a progressive, chronic infection may initiate new treatment options for this debilitating neurodegenerative disease.
http://chriskresser.com/
Alzheimer’s disease (AD) is a crippling, chronic, and progressive neurodegenerative disease that is conventionally understood to be irreversible. It is characterized by memory loss, dementia, cognitive impairment, and the presence of amyloid plaques in the brain (1, 2). Approximately 5.1 million people over the age of 65 in the United States are diagnosed with AD, along with another 200,000 under age 65. This estimate is predicted to increase by 10 million in the next 35 years (3).
In addition to those diagnosed, this disease changes the lives of more than 15 million family members and caregivers. Today, the estimated annual out-of-pocket expense plus the value of the approximately 18.1 billion volunteer caregiver hours approaches a staggering $440 billion (4). Unless there are advances in the cause and treatment of AD by the year 2050, that number will approach $1 trillion. The Centers for Disease Control & Prevention reports that AD is the sixth leading cause of death in the United States (4, 5). James et al. (2014) suggest that AD-related deaths are underreported and estimate that it is actually the third leading cause of death after heart disease and cancer (6).
Alzheimer’s disease was first characterized and diagnosed over 100 years ago (7). Since that time, ideas on the pathology and treatment of AD have shifted from a focus on amyloid plaques in the brain as the cause (8), to misfolded tau proteins (9), to focus on the genetic heritability of the disease, to epigenetic influences (10, 11), to inflammation as a primary culprit (2), to medication-induced mitochondrial dysfunction (12), and to metabolically influenced mechanisms (13, 14, 15).
The breadth of Alzheimer’s research speaks to how elusive this disease really is. Despite the uncertainty of specific causal mechanisms, there are currently five prescription drugs that are used to combat the symptoms of AD. The last drug approved to treat the symptoms of Alzheimer’s disease was brought on the market in 2003. Over the decade spanning 2002 to 2012, there were 413 AD drug trials performed; nearly four out of five of those clinical trials were sponsored by pharmaceutical companies. Trials were designed to test cognitive improvement, particular disease-modifying small molecules, and immunotherapies. The overall success rate over that period of time was measured to be 0.4 percent (99.6 percent failure) (1).
Recently, a group of 33 Alzheimer’s researchers joined forces to raise awareness about a neglected piece of the Alzheimer’s puzzle: the correlation between the manifestation of this disease and the microbial world (16).
An infectious disease is one that is caused by a pathogenic microbe and may be spread directly or indirectly (17). Infectious disease rates have plummeted over the course of the past century due to advances in sanitation, vaccination, and treatment (18). Historically, once a disease is identified to be infectious in origin, treatment and prevention protocols have been successful.
The idea that Alzheimer’s disease may be an infectious disease is supported by a number of observations. There have been many correlations between common infectious and immune-challenging agents and the diagnosis of AD (16).
Could Alzheimer’s be an infectious disease? Some research says yes.
“Seeding” Alzheimer’s disease in mice. Researchers have successfully created senile plaques associated with AD by infusing dilute fluid from the neocortex of Alzheimer’s patients into mice (19). These results highlight a key pathogenesis for neurodegenerative disease in mice and open up avenues for research in human subjects.
Type 2 diabetes and Alzheimer’s disease. A link between type 2 diabetes and AD has been suggested as both diseases present with local inflammation and amyloidosis (misfolded proteins) and are both associated with the presence of a common microbial community that includes Chlamydophyla pneumoniae, Helicobacter pylori, and spirochetes (20).
Periodontitis and Alzheimer’s disease. There is a correlation between the diagnosis of AD and periodontitis (21). Researchers hypothesize that the microbes living in dental plaque biofilm invade the brain via the bloodstream or peripheral nerves and promote inflammation of the central nervous system, which is known to be associated with cognitive decline (21, 22, 23).
Herpes simplex virus 1 and Alzheimer’s disease. Herpes simplex virus type 1 (HSV1) is quite common in the general population; roughly 70 percent of people over the age of 50 have been exposed to it. HSV1 was first proposed to be associated with AD nearly 35 years ago (24). This hypothesis was made plausible when researchers discovered a technique to test for the HSV1 virus in the human brain (25). After adjusting for known risk factors (age, education, APOE status) Letenneur et al. (2008) discovered a significant correlation between patients with primary or reactivated HSV1 (as measured by immunoglobulin M) and AD diagnosis (26, 27).
Atherosclerosis and Alzheimer’s disease. Atherosclerosis has been compared to AD because both diseases present with inflammation; are associated with viral and bacterial infection, including HSV1 and Chlamydophila; and are characterized by plaque formation. Researchers hypothesize that both are caused by a chronic immune challenge (infection) that induces cholesterol 25-hydroxylase expression (plaque) to protect the body locally against infectious agents (28).
Biotoxins and Alzheimer’s disease. A connection has been made between biotoxin exposure and a distinctive type of AD that affects younger people that is characterized by some combination of stroke-like speech impairment, partial Gerstmann’s syndrome, impaired ability to read, inability to interpret visual information, or impaired motor skills. This AD-type is “cortical” (14) and has now been reported in the literature as “inhalational Alzheimer’s disease” (IAD), a manifestation of chronic inflammatory response syndrome (CIRS) resulting from biotoxin exposure (29, 30).
Given the vast physical, mental, emotional, and financial burden that Alzheimer’s disease places on us, there is a dire need to be proactive. If the pathogenesis of AD includes an overlooked infectious component, there are many things that you can do starting today to decrease your odds of “contracting” this neurodegenerative disease.
It is not inaccurate to say that “health” is the best way to fight infection, but more specifically, a thriving, functioning immune system and a mindful perspective (31). An immune system under constant stress will slowly and steadily begin to malfunction over time, making our bodies more permissible to strange and pathogenic ecosystems (32, 33).
The best way to support your immune system and overall health is to provide your body with the information that it needs to operate and to make sure that the information delivered is in fact received. The receipt of this information is influenced by your overall gut health (34). Once gut health is considered, the required information from your environment comes from:
An “infectious disease” does not only manifest as an acute sickness; it may also manifest from chronic, progressive, and cumulative insults to the immune system over time.
Although I believe that Alzheimer’s (as well as most other modern diseases) is multifactorial and has several causes, the recognition that Alzheimer’s disease may be the result of a progressive, chronic infection may initiate new treatment options for this debilitating neurodegenerative disease.
http://www.marksdailyapple.com/
All fats are not created equal. We know this because we’re constantly correcting people who get it wrong. There are good fats and bad fats and really really bad fats and fats that are conditionally good or bad. Butter isn’t corn oil isn’t fish oil isn’t monounsaturated fat isn’t palmitoleic fat isn’t linoleic acid. Sometimes trans fat isn’t even trans fat. The same thing applies to the fat on your body. Depending on its location and composition, healthfulness isn’t distributed equally among adipose tissue. Some types of body fat are worse than others.
Fat is an endocrine organ. Like any other organ, it secretes hormones and other bioactive compounds that affect our physiology and determine our health.
Subcutaneous fat sits just below your skin. It’s the most conspicuous and least aesthetically-pleasing fat, comprising love handles and big droopy bellies, saggy arms and flabby necks, but it’s less actively harmful than many other types of body fat. Subcutaneous fat is the primary secretor of leptin, a strong regulator of appetite and metabolism, and of adiponectin, a marker for metabolic health with potentially anti-atherosclerotic effects.
Gluteofemoral fat is lower body fat, specifically the stuff that sits on your butt, hips, and thighs. In women, its presence indicates (and may even determine) good metabolic health. And it may not just be a signal for health, but an actor. Fat depots on the butt and hips actively secrete greater amounts of palmitoleic acid (PDF), a fatty acid with insulin-sensitizing effects. Gluteofemoral fat contains a greater proportion of omega-3 fatty acids, which are used to construct baby brains.
Visceral fat lies inside the abdominal cavity. It surrounds and envelops the organs. Contrasted with subcutaneous fat, visceral fat releases far less leptin and adiponectin. Instead, it secretes large amounts of IL-6, an inflammatory cytokine strongly correlated with systemic inflammation.
Intrahepatic fat is fat inside the liver. More than any other type of fat, intrahepatic fat is strongly associated with the metabolic complications of obesity.
Epicardial fat is visceral fat that surrounds the heart. If you’ve ever gotten a cow heart wrapped in hard yellowish fat, that’s epicardial fat. Large amounts of epicardial fat are associated with obesity, diabetes, and hypertension. And while epicardial fat appears to be primarily a signal of metabolic disturbances, it also exerts direct effects on heart function and releases inflammatory molecules that affect surrounding tissues.
Intermuscular fat lies between muscles. The less you use a muscle, the more it atrophies and the more fat will replace it. You may have seen the MRI of two thigh cross sections—one from a lifelong athlete and one from an age-matched couch potato. The athlete’s leg is a dense circle of bone surrounded by several inches of lean muscle in each direction followed by a small layer of fat. The sedentary leg is smaller circle of bone surrounded by a mishmash of marbled meat with several inches of thick white fat. Delicious and tender when seared, I’d imagine, but terrible for the person’s health and ability to function.
Intramuscular fat lies inside the muscles. Kobe beef steaks have lots of intramuscular fat. It’s the marbling, the presence of fat between muscle fibers. If you actually utilize it, intramuscular fat provides a nice source of energy for the muscles. Then again, if you were using your muscles in the first place it’d be tough to accumulate much intramuscular fat. The quickest way to get rid of intramuscular fat is with low-level aerobic activity. Staying under 75% of max heart rate will keep you burning predominately fat, and exercising while on a ketogenic diet is an even better way to do it; nutritional ketosis increases exercise-induced intramuscular fat oxidation 20-fold.
Brown fat isn’t really fat. It is, but it isn’t. Like muscle, it’s highly metabolically active. We use it to generate heat (thus burning energy) in response to cold exposure. Babies have a ton of brown fat, since they can’t shiver to stay warm, and until recently researchers assumed adults didn’t have much at all. Now we know that’s wrong. Cold plunges, swimming in cool water, and even going outside in short sleeves and shorts in cold weather can all stimulate the formation of brown fat in adults (I wouldn’t advise dunking your newborn in an ice bath for the health benefits). Those jerk babies aren’t the only ones enjoying that sweet, sweet brown fat after all.
Best of all, “training” for brown fat—in one study, exposing yourself to cool weather (60°F) for just 2 hours a day for six weeks while wearing light clothing—can increase energy expenditure and reduce overall body fatness. That’s not even a big dose of cold. Forgetting your jacket at home is probably enough.
Different populations have different body fat distribution patterns. Let’s look at a few:
South Asians (Indians, Pakistanis, Bangladeshis) have smaller subcutaneous “reservoirs” than whites, so a larger proportion of weight gain in this population diverts to visceral—and more dangerous—fat stores. Dr. Ron Sinha wrote about this (and still does on his blog) in the fantastic South Asian Health Solution.
Compared to Australian whites, Japanese men have more body fat for a given BMI.
Black Americans have less visceral fat and more subcutaneous fat for a given BMI than white Americans (PDF). Oddly, this doesn’t translate to a lower risk of diabetes.
Australian Aborigines have more trunk fat and less limb fat for a given BMI than Australians of European descent. Aborigine women have higher waist circumferences and waist:hip ratios than Aussie European women for a given BMI.
Men and women carry fat differently. I mentioned that briefly above in the section on gluteofemoral fat, and I covered the differences extensively in a previous post. Go read that now. In short, men are more likely to store fat on the trunk and around the waist, leading to the fat-guy-with-stick-legs syndrome. Women tend to store fat in the butt, thighs, and hips. Upon reaching menopause, women stop producing as much estrogen and begin storing more fat in the waist and abdomen.
The eternal question persists: is it cause or signal? Risk factor or actor? For most of these types of fat, the answer is probably “both.” Fatty liver indicates metabolic dysfunction, but it can also impair the liver’s functions and lead to insulin resistance and eventually diabetes. People with lots of brown fat may be lean and healthy because they spend a lot of time being active in cold weather, but the brown fat also increases caloric expenditure. Large amounts of intramuscular and epicardial fat indicate a sedentary lifestyle, which is damaging in its own right, but the fat secretes inflammatory compounds with real biological effects.
Teasing apart which link along the chain of causality is to blame is probably impossible. That doesn’t mean we can’t make a few safe recommendations.
Women shouldn’t stress out about a little butt, hip, and thigh fat. It’s likely a good sign.
Belly fat is bad. Fat around your heart is bad. Fat in your liver is bad. Subcutaneous fat looks bad and is hardest to burn but might not be too unhealthy. Losing weight will reduce all of it.
To target belly fat, intense training works best. The resultant spike in catecholamines will preferentially target visceral fat. Just be sure to get enough sleep, rest, and recovery, as chronic stress and under-recovery tends to chronically elevate the catecholamines and make belly fat more stubborn.
To target liver fat, limit sugar, eat lots of choline (from yolks and liver), and practice high intensity interval training. When you drink alcohol, make sure you protect your liver with saturated fat (beef, cocoa, coconut fat all protect against alcohol-induced fatty liver).
To target intramuscular fat, exercise in a low-carb or ketogenic state. Nothing too intense is required. A long, reasonably intense hike (lots of hills) on an empty stomach twice a week might do the trick.
To target epicardial fat, exercise. Both intense and moderate-intensity training seem to work.
To get more brown fat, forget your jacket. Heck, burn it. Just don’t stand too close to the fire.
If it sounds confusing, it shouldn’t. The basics apply. Recommendations haven’t changed. I just find all the different types of fat incredibly interesting. Don’t you?
Thanks for reading, everyone. Take care and be sure to let me know what you think about all this.
http://www.thekitchn.com/feedburnermain
If you’ve been a lifelong omnivore, going vegan is no easy feat. But if you find yourself deciding that a vegan way of eating is for you, you’re going to need recipes. These 17 vegan recipes are so surprising and delicious that going vegan might just be easier than you think.
Originally Posted At: https://breakingmuscle.com/feed/rss
I read two articles recently that got me thinking about the modern state of parenting. One was titled, “We Don’t Allow Children to Climb Trees.” It was a discussion of new restrictions put in place by early childhood education providers in Norway.
http://www.thekitchn.com/feedburnermain
My culinary experience with clams is pretty limited. I’ve only prepared them once, and — truthfully — I didn’t particularly care for them. The real fun, I find, is in hunting for them on the beach. When I was quite young, my dad taught me to spot hiding clams by the telltale thumbprint-shaped indents they leave in the sand. We always tossed them back into the water, but it was fun to unearth a few, just because, with a few gentle scrapes into the wet sand.
The mollusks I’m familiar with were always speckled very sparingly across the beach. These ones, however … let’s just say their placement is quite generous. Watch for yourself.
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