Showing posts with label disease - inflamation. Show all posts
Showing posts with label disease - inflamation. Show all posts

1.7.11

Saturated fat Study (1997) - An Example of Junk Science

Low Carbohydrate Nutrition: An Example of Junk Science

Extract:

An Example of Junk Science

By Mary Enig Phd


While the establishment is finally recognizing the dangers of trans fatty acids, conventional dietary gurus continue to warn the public about the alleged dangers of saturated fats.

In this article, we will look at a study published in 1997 in the American Journal of Cardiology (79:350-354) used to justify avoidance of red meat and butterfat, the two main sources of saturated fatty acids in the Western diet.

Arthur Agatston, author of the best-selling South Beach Diet refers to this research when he states:
"The major problem I have with the Atkins Diet is the liberal intake of saturated fats. There is evidence now that immediately following a meal of saturated fats, there is dysfunction in the arteries, including those that supply the heart muscle with blood. As a result, the lining of the arteries (the endothelium) is predisposed to constriction and clotting. Imagine: Under the right (or rather, wrong) circumstances, eating a meal that’s high in saturated fat can trigger a heart attack! In addition, after a high-fat meal certain elements in the blood called remnant particles, persist for longer than is healthy. These particles contribute to the buildup of plaque in the vessel wall."
Agatston recommends consuming polyunsaturated and monounsaturated vegetable oils, including tub spreads, rather than animal fats like butter.

In the study, carried out by Robert A. Vogel and his team at the University of Maryland School of Medicine, ten volunteers were tested for "endothelial function" by measuring.....[  ].

But was it saturated fat that caused the decline in endothelial function?

The high-fat meal consisted of an egg McMuffin, sausage McMuffin, two hash brown patties and a noncaffeinated beverage. The lowfat meal consisted of Frosted Flakes, skimmed milk and orange juice. According to the authors, the high fat meal contained 50 grams of fat, of which 14 were saturated fat. So only 28 percent of the fat in the high-fat meal was saturated. The rest was a combination of trans fats, monounsaturated and polyunsaturated fat, any one of which, or all together are the likely culprits in the decline in endothelial function.

But Agatston (along with the study authors) blames the adverse effects on saturated fats!

28.6.11

Arthritis & psoriasis medications - reduced diabetes risk

Common rheumatoid arthritis and psoriasis medications are associated with reduced diabetes risk

Common Rheumatoid Arthritis and Psoriasis Medications Are Associated With Reduced Diabetes Risk

ScienceDaily (June 22, 2011) — Individuals with systemic inflammatory conditions, such as rheumatoid arthritis (RA) and psoriasis, experience a 1.5 to 2-fold increased rate of cardiovascular disease. Previous research suggests that inflammation and insulin resistance, linked with these conditions, likely accelerate the development of cardiovascular risk and diabetes. Researchers at Brigham and Women's Hospital (BWH) sought to determine whether commonly used disease-modifying antirheumatic drugs (DMARDs), which are directed against inflammation, might reduce the risk for developing diabetes in patients with RA or psoriasis.

They found that among patients with RA or psoriasis, the risk for developing diabetes was lower for those patients who started TNF inhibitor or hydroxychloroquine.

Their findings are published in the June 22/29, 2011 issue of the Journal of the American Medical Association.

27.6.11

Study - inflammation in fat tissue after overeating

Short-term overfeeding may induce peripheral insul... [Diabetes. 2010] - PubMed result

Diabetes. 2010 Sep;59(9):2164-70. Epub 2010 Jun 14.

Short-term overfeeding may induce peripheral insulin resistance without altering subcutaneous adipose tissue macrophages in humans.

Source

Diabetes & Obesity Research Program, Garvan Institute of Medical Research, Sydney, Australia.

Abstract

OBJECTIVE:

Chronic low-grade inflammation is a feature of obesity and is postulated to be causal in the development of insulin resistance and type 2 diabetes. The aim of this study was to assess whether overfeeding induces peripheral insulin resistance in lean and overweight humans, and, if so, whether it is associated with increased systemic and adipose tissue inflammation.

RESEARCH DESIGN AND METHODS:

Thirty-six healthy individuals undertook 28 days of overfeeding by +1,250 kcal/day (45% fat). Weight, body composition, insulin sensitivity (hyperinsulinemic-euglycemic clamp), serum and gene expression of inflammation markers, immune cell activation, fat cell size, macrophage and T-cell numbers in abdominal subcutaneous adipose tissue (flow cytometry and immunohistochemistry) were assessed at baseline and after 28 days.

RESULTS:

Subjects gained 2.7 +/- 1.6 kg (P < 0.001) and increased fat mass by 1.1 +/- 1.6% (P < 0.001). Insulin sensitivity decreased by 11% from 54.6 +/- 18.7 to 48.9 +/- 15.7 micromol/(kg of FFM)/min (P = 0.01). There was a significant increase in circulating C-reactive protein (P = 0.002) and monocyte chemoattractant protein-1 (P = 0.01), but no change in interleukin-6 and intercellular adhesion molecule-1. There were no changes in fat cell size, the number of adipose tissue macrophages or T-cells, or inflammatory gene expression and no change in circulating immune cell number or expression of their surface activation markers after overfeeding.

CONCLUSIONS:

Weight gain-induced insulin resistance was observed in the absence of a significant inflammatory state, suggesting that inflammation in subcutaneous adipose tissue occurs subsequent to peripheral insulin resistance in humans.

PMID:
20547978
[PubMed - indexed for MEDLINE]
PMCID: PMC2927938
[Available on 2011/9/1]
Free full text

LinkOut - more resources

26.6.11

Nuts - effect on inflammation, PubMed

The effect of nuts on inflammation. [Asia Pac J Clin Nutr. 2008] - PubMed result

Asia Pac J Clin Nutr. 2008;17 Suppl 1:333-6.

The effect of nuts on inflammation.

Source

Human Nutrition Unit, Department of Biochemistry and Biotech-nology, Faculty of Medicine and Health Sciences, Universitat Rovira i Virgili, C/Sant Llorenc, 21, 43201 Reus, Spain. jordi.salas@urv.cat

Abstract

Inflammation is one of the recognised mechanisms involved in the development of atherosclerotic plaque and insulin resistance. Inflammatory or endothelial markers such as C-Reactive Protein (CRP), Interleukin-6 (IL-6), fibrinogen, Vascular Cell Adhesion Molecule-1 (VCAM-1) and Intracellular Adhesion Molecule-1 (ICAM-1) have been identified as independent predictors of cardiovascular disease (CVD) or diabetes in human prospective studies. Epidemiological and clinical studies suggest that some dietary factors, such as n-3 polyunsaturated fatty acids, antioxidant vitamins, dietary fiber, L-arginine and magnesium may play an important role in modulating inflammation. The relationship observed between frequent nut consumption and the reduced risk of cardiovascular mortality and type 2 diabetes in some prospective studies could be explained by the fact that nuts are rich in all of these modulator nutrients. In fact, frequent nut consumption has been associated with lower concentrations of some peripheral inflammation markers in cross-sectional studies. Nut consumption has also been shown to decrease the plasma concentration of CRP, IL-6 and some endothelial markers in recent clinical trials.
PMID:
18296371
[PubMed - indexed for MEDLINE]

25.6.11

Omega 3 - Precious Yet Perilous (intro)

Precious Yet Perilous
Written by Chris Masterjohn Phd
September 22 2010 15:02

Extracts:

Even in adulthood, however, dietary fats influence the DHA concentrations of most other tissues. Recent research has shown that our tissues use DHA to synthesize compounds called “resolvins,” which are involved in bringing inflammatory responses to an end when they are no longer needed.51

 Sufficient DHA thus allows the immune system to mount a robust inflammatory response against invading pathogens or damaged tissues and to bring the response quickly to an end once the task has been accomplished. Researchers are increasingly discovering that most degenerative diseases involve an element of chronic, low-level inflammation, and the inability to “turn off” important inflammatory processes once they are no longer needed could be part of the problem. DHA deficiency may therefore be at the root of widespread declines in cognitive function, increases in mental disorders and epidemic levels of degenerative disease.

EPA, a precursor to DHA, is an omega-3 fatty acid that accumulates in fish but generally exists in only infinitesimal quantities in mammals and other land animals. Many authors consider EPA an “anti-inflammatory” essential fatty acid, but its “anti-inflammatory” activity is a result of its ability to interfere with arachidonic acid metabolism.

The conversion of arachidonic acid to PGE2 in immune cells is an important initiator of inflammation, but it also turns on the genes necessary for the synthesis of compounds that resolve inflammation, some of which are derived from arachidonic acid and others of which are derived from DHA.52 Providing sufficient DHA to allow the synthesis of the full spectrum of inflammation-resolving compounds is a nutritional approach to inflammation. Providing high doses of EPA that interfere with arachidonic acid metabolism, however, is a pharmacological approach, and it is likely to have many adverse consequences.

Omega 6/Omega 3 Ratio - Precious Yet Perilous

Precious Yet Perilous
Written by Chris Masterjohn Phd

The Omega -6-to -Omega -3 Ratio

An often-cited animal experiment suggested that the ideal ratio of omega-6 linoleic acid to omega-3 ALA is four-to-one, but this experiment injected rats with free fatty acids rather than feeding them dietary oils.47 A more realistic experiment that fed rats a mix of various vegetable oils in a broad range of different proportions showed that a ratio of nine-to-one maximized tissue DHA content just as well as lower ratios.48 The precise ratio is likely to be of much less importance, however, when there is preformed arachidonic acid and DHA in the diet. Nevertheless, people who consume the standard American diet rich in vegetable oils may face adverse consequences from consuming excess linoleic acid and people who consume large amounts of fatty fish, fish oil or cod liver oil may face adverse consequences from consuming an excess of the omega-3 fatty acid eicosapentaenoic acid (EPA).
Among ten populations studied from five different continents, American adults have the highest blood levels of omega-6 fatty acids and American infants have the lowest blood levels of omega-3 fatty acids.33 Up until the 1930s, Americans consumed on average about 15 grams (one tablespoon) of PUFA per day. Since the 1930s, this value has more than doubled to over 35 grams per day as Americans have increased their intake of vegetable oils rich in the omega-6 linoleic acid (see Figure 2).2 Most of this increase occurred after 1961 when the American Heart Association began recommending that people replace saturated fats with vegetable oils in order to lower cholesterol levels.3
Similar increases in linoleic acid have been shown to decrease the conversion of ALA to longer-chain omega-3 fatty acids such as DHA in humans.49 Human studies tend to look at the fatty acids incorporated into red blood cells, but animal experiments provide much more detailed information about the concentrations of fatty acids in the organs and glands where they are most needed. These experiments show that excesses of linoleic acid do not increase tissue concentrations of arachidonic acid; instead, they replace the true omega-3 DHA with a “fake” omega-6 version of DHA that ordinarily is not found in substantial amounts within the body.50 The main effect of the excess linoleic acid in the standard American diet is thus most likely to be a mild form of DHA deficiency.
The effect of excess linoleic acid is probably most detrimental to infants and young children whose brains are still developing. DHA deficiency during early development may have lasting effects on cognitive and visual function during adulthood. Animal experiments even suggest that these effects are multi-generational, with the DHA concentration of nervous tissue declining with each successive generation.
Even in adulthood, however, dietary fats influence the DHA concentrations of most other tissues. Recent research has shown that our tissues use DHA to synthesize compounds called “resolvins,” which are involved in bringing inflammatory responses to an end when they are no longer needed.51 Sufficient DHA thus allows the immune system to mount a robust inflammatory response against invading pathogens or damaged tissues and to bring the response quickly to an end once the task has been accomplished. Researchers are increasingly discovering that most degenerative diseases involve an element of chronic, low-level inflammation, and the inability to “turn off” important inflammatory processes once they are no longer needed could be part of the problem. DHA deficiency may therefore be at the root of widespread declines in cognitive function, increases in mental disorders and epidemic levels of degenerative disease.
EPA, a precursor to DHA, is an omega-3 fatty acid that accumulates in fish but generally exists in only infinitesimal quantities in mammals and other land animals. Many authors consider EPA an “anti-inflammatory” essential fatty acid, but its “anti-inflammatory” activity is a result of its ability to interfere with arachidonic acid metabolism. The conversion of arachidonic acid to PGE2 in immune cells is an important initiator of inflammation, but it also turns on the genes necessary for the synthesis of compounds that resolve inflammation, some of which are derived from arachidonic acid and others of which are derived from DHA.52 Providing sufficient DHA to allow the synthesis of the full spectrum of inflammation-resolving compounds is a nutritional approach to inflammation. Providing high doses of EPA that interfere with arachidonic acid metabolism, however, is a pharmacological approach, and it is likely to have many adverse consequences.
When Holman and Widmer first discovered the dichotomy between omega-3 and omega-6 fatty acids, they examined nine different tissues in rats on normal lab diets and could not find even a trace of EPA unless they had first induced essential fatty acid deficiency and all its related tissue damage.32 Several years later Holman conducted a study with another colleague showing that ALA aggravated essential fatty acid deficiency; if they gave the animals vitamin B6, however, the rats converted ALA to DHA rather than to EPA and the aggravating effect disappeared.19 More recent studies in humans have provided preliminary evidence suggesting that EPA interferes with growth in infants and immune function in adults, while DHA improves both growth and immune function.53-54
fall10-masterjohnfigure2Figure 2. Increase in American PUFA Consumption
Consumption of polyunsaturated fat in
the United States between 1909 and
2005 based on USDA food disappearance
data. From reference 2,
courtesy of Stephan Guyenet’s Whole
Health Source blog
(used with permission).
John Hughes Bennett, a nineteenth century Scottish physician who traveled the world studying the use of cod liver oil in medicine, wrote in his Treatise on Cod Liver Oil that excessive doses over extended periods of time could cause gastrointestinal problems, excessive menstrual bleeding, itchy skin eruptions and excessive evaporation of water through the skin.55 The last three symptoms seem very much like the hormonal disruptions, hemorrhaging and skin problems known to occur during arachidonic acid deficiency. Had the Burrs looked for gastrointestinal disorders during essential fatty acid deficiency, they probably would have found them. Non-steroidal anti-inflammatory drugs (NSAIDs) work their magic by interfering with the production of PGE2 from arachidonic acid, a characteristic they share with EPA. One of the most common set of side effects associated with these drugs is gastrointestinal disturbances. Four out of ten users of NSAIDs experience symptoms such as heartburn, acid reflux, stomach burning, nausea, or bloating.56 Researchers have used NSAIDs to produce food intolerances in mice that result in a form of severe intestinal damage called villous atrophy that is usually associated with celiac disease,57 suggesting that a deficiency of arachidonic acid or the PGE2 made from it may underlie celiac disease and other food intolerances, perhaps by preventing the gut from forming cellular junctions and thus impairing its integrity. Excessive doses of EPA from fatty fish, fish oil and cod liver oil may contribute to all of these symptoms in susceptible individuals.
Our bodies use the same enzymes to convert EPA to DHA as they use to convert ALA to DHA or linoleic acid to arachidonic acid. The same conditions that reduce the requirement for arachidonic acid and DHA are likely to increase a person’s tolerance for EPA. A diet that excludes refined sugar and rancid vegetable oil, is low in total PUFA content, is adequate in protein and total energy, and is rich in vitamin B6, biotin, calcium, magnesium, and fresh, whole foods abundant in natural antioxidants should not carry any risk of arachidonic acid deficiency when moderate amounts of EPA are consumed. Liberal amounts of egg yolks and liver providing preformed arachidonic acid would provide extra insurance against damage by EPA. Under these conditions, it would be safe to consume cod liver oil—valuable for its abundant provision of DHA, vitamin A and vitamin D—in spite of its EPA content.

too much omega-6, not enough omega-3 - making us sick

How too much omega-6 and not enough omega-3 is making us sick

Death by vegetable oil

So what are the consequences to human health of an n-6:n-3 ratio that is up to 25 times higher than it should be?
The short answer is that elevated n-6 intakes are associated with an increase in all inflammatory diseases – which is to say virtually all diseases. The list includes (but isn’t limited to):
  • cardiovascular disease
  • type 2 diabetes
  • obesity
  • metabolic syndrome
  • irritable bowel syndrome & inflammatory bowel disease
  • macular degeneration
  • rheumatoid arthritis
  • asthma
  • cancer
  • psychiatric disorders
  • autoimmune diseases
The relationship between intake n-6 fats and cardiovascular mortality is particularly striking. The following chart, from an article entitled Eicosanoids and Ischemic Heart Disease by Stephan Guyenet, clearly illustrates the correlation between a rising intake of n-6 and increased mortality from heart disease:
landis graph of hufa and mortality
As you can see, the USA is right up there at the top with the highest intake of n-6 fat and the greatest risk of death from heart disease.

Fish oil, inflammation & disease - Dr. Barry Sears

Dr. Barry Sears speaks about fish oil and inflammation.




Uploaded by on Oct 17, 2009, from www.crossfit.com

Mediators of Inflammation — An Open Access Journal

Mediators of Inflammation — An Open Access Journal

About this Journal 

Mediators of Inflammation is a peer-reviewed, open access journal that publishes original research and review articles on all types of inflammatory mediators, including cytokines, histamine, bradykinin, prostaglandins, leukotrienes, PAF, biological response modifiers and the family of cell adhesion-promoting molecules.

The most recent Impact Factor for Mediators of Inflammation is 2.019 according to 2009 Journal Citation Reports released by Thomson Reuters (ISI) in 2010.

Study (2004) - paradox how saturated fat prevents coronary artery disease

Saturated fat prevents coronary artery disease? An American paradox

American Journal of Clinical Nutrition, Vol. 80, No. 5, 1102-1103, November 2004
© 2004 American Society for Clinical Nutrition

EDITORIAL

Saturated fat prevents coronary artery disease? An American paradox1,2

Robert H Knopp and Barbara M Retzlaff
1 From the Northwest Lipid Research Clinic, University of Washington School of Medicine, Seattle

In conclusion, the hypothesis-generating report of Mozaffarian et al draws attention to the different effects of diet on lipoprotein physiology and cardiovascular disease risk. These effects include the paradox that a high-fat, high–saturated fat diet is associated with diminished coronary artery disease progression in women with the metabolic syndrome, a condition that is epidemic in the United States. This paradox presents a challenge to differentiate the effects of dietary fat on lipoproteins and cardiovascular disease risk in men and women, in the different lipid disorders, and in the metabolic syndrome.

23.6.11

Omega 6 - Many Medications work by Blocking Omega-6

Omega-6 Fat Research News & Commentary: Medications that Block Effects of Omega-6 Fat

Medications that Block Effects of Omega-6 Fat

Bottomline: Arachidonic acid , the potent omega-6 fat, creates health-harming inflammatory chemicals in the body. Many anti-inflammatory medications such as aspirin, Celebrex and Singulair work by blunting the effects of omega-6 fat.


Many of the health benefits derived from omega-3 fats in fish oil (EPA and DHA) are from their ability to block the harmful effects of arachidonic acid. Arachidonic acid is the most problematic of the omega-6 fats and is found in animal products. The plant omega-6 fat, linoleic acid, commonly found in vegetable oils (especially soybean oil, cottonseed oil, and corn oil), easily gets made into arachidonic acid by the body.

Omega 6 Asthma Triggers also Clog Arteries

Omega-6 Fat Research News & Commentary: Asthma Triggering Compounds from Omega-6 Fat Create Clogged Arteries

Asthma Triggering Compounds from Omega-6 Fat Create Clogged Arteries

Bottomline: Excellent review paper, which describes how the potent inflammatory compounds, which trigger asthma, also damage arteries, via the leukotrienes generated from the omega-6 fat, arachidonic acid. Cardiovasc Drugs Ther. 2008 Oct 24. [Epub ahead of print]








Summary: This review paper describes the accumulating body of evidence, demonstrating how leukotrienes, the powerful group of eicosanoids, infamous for damaging lungs and triggering asthma, are also involved in heart disease. The key stages of arterial damage are described, beginning with irritation of the blood vessels linings, resulting in plaque accumulation and ultimately the potentially deadly rupture of the plaque (as depicted above).

Omega-6 & 3 Impact Your Inflammation Gene Machine

Omega-6 Fat Research News & Commentary: Dietary Fats Omega-6 and Omega-3: Impact Your Inflammation Gene Machine

Dietary Fats Omega-6 and Omega-3: Impact Your Inflammation Gene Machine

Bottomline: The first human study shows that modifying diet changes the cellular levels of omega-6 and omega-3 polyunsaturated fatty acids, which directly impact inflammation genes. J Biol Chem. 2009 Jun 5;284(23):15400-7.

Background: Inflammatory diseases are on the rise. It is estimated that within the next two decades, more than one in three Americans will have an inflammatory disease, which include heart disease, asthma and rheumatoid arthritis. Many scientists believe this upward trend is due to the dramatic rise in dietary omega-6 polyunsaturated fats, which outnumber omega-3 fats, by 10 to 1, in the typical American diet. In contrast, our hunter-gatherer ancestors consumed an estimated one-to-one balance of these fats.

Studies indicated that eating excess dietary omega-6 fat, increases the omega-6 derived eicosanoids, (which include leukotrienes); which in turn, may lead to a systemic pro-inflammatory state in the body. For example, when the LOX enzyme acts on the omega-6 fatty acid, arachidonic acid, it creates the potent leukotriene, LTB4, (which is the compound implicated in asthma and atherosclerosis). Yet, if this enzyme acts on the omega-3 fatty acid, EPA, it creates leukotriene compounds that are 10 to 100-fold less potent.

Additionally, animal studies indicate that polyunsaturated fatty acids modulate the genes effecting inflammation. But whether that holds true for people, has been unknown, until this study
.

Type 3 Diabetes - Brain Diabetes?

USPharmacist.com > Type 3 Diabetes: Brain Diabetes?

Type 3 Diabetes: Brain Diabetes?

A relationship between diabetes mellitus (DM) and dementia is undeniable, with numerous studies concluding that DM increases the risk of cognitive decline and dementia, including Alzheimer’s disease (AD).1-5 Not only does DM increase the risk of dementia, it actually increases the rate of dementia development two- to threefold.3

The mechanism of this impairment is not fully understood, but it is hypothesized that hyperglycemia, insulin resistance, oxidative stress, advanced glycation end products, and inflammatory cytokines collectively lead to cognitive dysfunction.5

In fact, diabetes was described as a “special kind of accelerated aging” in 1976 owing to its many associated complications.5

The apparent overlap between DM and dementia has led to the suggestion that AD is not solely a neurologic disorder, but rather a neuroendocrine disorder, with Steen et al coining the term type 3 diabetes to describe this hybrid disease.6

11.6.11

Glycation - causes disease and aging

Phd nutritional biochemist and bodybuilder Dr. Greg Ellis has written a book titled "The Glycation Factor". he says that carbs interact with protein and this leads to glycation, inflammation and disease. atherosclerosis in diabetics (ie blood sugar too high) is known to be caused via glycation - see 50kzone: Glycation, heart disease and cancer










detailed interview with Ellis at the Jimmy Moore podcast website here - 461: Dr. Greg Ellis Tells Clients To Say ‘Bye Bye, Carbs! and here

body builder website interview with Ellis here: http://www.bodybuilding.com/fun/mahler11.htm

Dr Greg Ellis's You Tube video library linked here: http://www.youtube.com/user/Byebyecarbs#g/u

Interviewed here: http://www.youtube.com/user/bionicbrown#g/search

9.6.11

Omega 6, Eicosanoids, Inflammation, Cortisol, and Syndrome X

Matt Stone - from the 180 Degree Health blog (hear him interviewed by Jimmy Moore here).

brief podcast on omega 6 fatty acids - a footnote to an earlier post on topic (reproduced below), reinforcing why accumulating a lot of omega 6 in our tissues may be a really, really big deal with all kinds of negative repercussions.

6.6.11

Inflammatory Foods - video on Harvard Health Studies

Dr. Youngberg discusses the Harvard Health Studies that outline the four most inflammatory and therefore disease causing food groups.  This is a clip from "Turning off the Fat Gene" which is one of thee presentations on the "Controlling Cravings with Contentment DVD series.


5.6.11

Inflammation - as a Target for Anti-cancer Therapy


UCSF professor of Pathology Lisa Coussens explores inflammation as a target for anti-cancer drugs. Series: "Inflammation as Cause and Consequence of Disease" [2/2008] [Health and Medicine] [Show ID: 13575]

Inflammation - and Immunity and Diabetes


Jeffrey Bluestone, director of the diabetes center at UCSF explores the impact if inflammation and immunity on diabetes. Series: "Inflammation as Cause and Consequence of Disease" [2/2008] [Health and Medicine] [Show ID: 13580]

Inflammation - new understanding of disease

Andrew Chan of Genentech explores new therapies for inflammatory diseases Series: Inflammation as Cause and Consequence of Disease [1/2008] [Health and Medicine] [Professional Medical Education] [Show ID: 13581]