Categories:

Master List: Ray Peat, PhD Interviews

Also see:
Collection of Ray Peat Quote Blogs by FPS

This blog stores an ever expanding list of interviews with Ray Peat, PhD. Special thanks to Angela de Souza, Tyler Derosier, Dan Wich, and other commenters for helping me accumulate the material. Will update as more interviews become available. Contact me if any links are fudged up or not working – Rob@functionalps.com. If you’re going to use this list on your blog, please provide citation.

FPS coaches a 12 week nutrition course based solely on the methodology of Ray Peat, PhD. Please click here for more information.

Ray Peat Search Engine:
L-I-G-H-T

Video/Audio Interviews:



Written Interviews:
Organizing the Panic – An Interview with Dr. Ray Peat
Dr. Raymond Peat — Thyroid Information
Ray Peat – A Renowned Nutritional Counselor’s Thoughts About Thyroid Disease
An Interview With Dr. Raymond Peat
An Interview With Dr. Raymond Peat Part II: Mind & Body
Ray Peat Interviews Revisited
Transcription of NPR Interview: The Thyroid (1996)
Ray Peat on Negation (2014)
On culture, government, and social class (2016)

Quote Compilations:
Multiple Audio Interviews on Youtube

Collection of Ray Peat Quote Blogs by FPS
Email exchanges with Ray Peat – Compilation
Ray Peat’s Brain: Building A Foundation For Better Understanding
Ray Peat’s Brain Part II: An Index Of Terms & Ideas

Ray Peat Email Advice Depository
PeatSearch by Dan Wich

Ray Peat Book Quotes – 180 Degree Health

Audio Interviews:
Various Audio Interview Transcripts

Generative Energy: Talking with Ray Peat (NEW 2016)

Herb Doctors: Endocrine (Glands/Hormones) System, Parkinson’s (NEW 2017)
Herb Doctors: The Precautionary Principle Part II (NEW 2017)
Herb Doctors: The Precautionary Principle Part I (NEW 2017)
Herb Doctors: Food Choice (NEW 2016)
Herb Doctors: Vitamin D (NEW 2016)
Herb Doctors: Rheumatoid Arthritis (NEW 2016)
Herb Doctors: Antioxidant Theory and the Continued War on Cancer (NEW 2016)
Herb Doctors: Cancer Metabolism, Lactic Acid, Carbon Dioxide, Sugar Deprivation Promotes Cancer (NEW 2016)
Herb Doctors: Authoritarianism, Politics, 2016 US Election (NEW 2016)
Herb Doctors: Exploring Alternatives (NEW 2016)
Herb Doctors: Mitochondrial Support, Stress, GABA, Herbs (NEW 2016 – show starts at 9:06)
Herb Doctors: Allergy (Cholesterol, PUFA, Prostaglandins, Energy, Blood Glucose, Stress) (NEW 2016)
Herb Doctors: Iodine, Supplement Reactions, Hormones, and More (NEW 2016)
Herb Doctors: Water Quality, Chlorinated Water, Global Warming, Deforestation (NEW 2016)
Herb Doctors: Nitric Oxide, Nitrates, Nitrites, Flouride, Fertility (2015)
Herb Doctors: Rudolph Steiner Schools, Biodynamic Agriculture, Education (2015)
Herb Doctors: Nitric Oxide Part 2 (2015)
Herb Doctors: Longevity and Brain Food (2015)
Herb Doctors: Urea (2015)
Herb Doctors: Degradation of the Food Supply; Vaccines (2015)
Herb Doctors: Breast Cancer (2015)
Herb Doctors: Digestion and Emotion (2015)
Herb Doctors: You are what you eat (2014)
Herb Doctors: Nitric Oxide (2014)
Herb Doctors: Longevity (2014)
Herb Doctors: Field Biology (2014)
Herb Doctors: Thinking Outside the Box – Cancer Treatment (2014)
Herb Doctors: Vaccines & Immunity 2 (2014)
Herb Doctors: Vaccines & Immunity 1 (2014)
Herb Doctors: Cognition and Memory (2014)
Herb Doctors: Partial Interview (2014)
Herb Doctors: Diabetes, Neuropathy (2014)
Herb Doctors: Various Topics, Q&A (2014)
Herb Doctors: Aging and Energy (2013)
Herb Doctors: Hashimotos Thyroiditis, Temperature, Pulse Rate (2013)
Herb Doctors: Autonomic Nervous System (2013)
Herb Doctors: Environmental Enrichment & The Brain (2013)
Herb Doctors: Heart, Hormones, Cancer, and Eyes (2013)
Herb Doctors: The Heart and Dietary Fats (2013)
Herb Doctors: The Heart and Hormones (2013)
Herb Doctors: The Heart, Palpitations, Progesterone, Estrogen (2013)
Herb Doctors: Weight Loss (2013)
Herb Doctors: Carbon Monoxide (2013)
Herb Doctors: Learning, Dementia, Alzheimers (2012)
Herb Doctors: Ionizing and Non-Ionizing Radiation (2012)
Herb Doctors: Antioxidants (2012)
Herb Doctors: Inorganic Phosphates, Calcium:Phosphorus Ratio, & Aging (2012)
Herb Doctors: Blood Pressure Regulation Heart Failure and Muscle Atrophy (2012)
Herb Doctors: Cellular Repair (2012)
Herb Doctors: Genetic Determinism (2012)
Herb Doctors: Alkalinity vs Acidity (2012)
Herb Doctors: Cancer Treatment (2012)
Herb Doctors: Sodium/Salt, Inflammation, Pregnancy Toxemia, Water Retention (2011)
Herb Doctors: Energy Production, Diabetes, and Saturated Fats (2011)
Herb Doctors: Sugar II (2011)
Herb Doctors: Sugar I, Cholesterol, Obesity, Heart Disease (2011)
Herb Doctors: Fukushima I (2011)
Herb Doctors: Fukushima II, Serotonin, & Melatonin (2011)
Herb Doctors: Endotoxin (2010)
Herb Doctors: Hair loss, Osteoporosis
Herb Doctors: Inflammation
Herb Doctors: Milk
Herb Doctors: Radiation (2010)
Herb Doctors: Serotonin, Endotoxins, and Stress
Herb Doctors: Altitude and CO2 (2010)
Herb Doctors: Sugar Part 1 (2010)
Herb Doctors: Sugar Part 2 (2010)
Herb Doctors: Hormones, Metabolism
Herb Doctors: Misconceptions about Serotonin and Melatonin
Herb Doctors: Food Additives (2009)
Herb Doctors: The Ten Most Toxic Things In Our Food (2009)
Herb Doctors: You Are What You Eat (2009)
Herb Doctors: Bowel Endotoxin (2009)
Herb Doctors: Thyroid, Polyunsaturated Fats, and Oils (2009)
Herb Doctors: Cholesterol is an Important Molecule (2008)
Herb Doctors: Thyroid, Metabolism, and Coconut Oil Part 2 (2008)
Herb Doctors: Thyroid, Metabolism, and Coconut Oil Part 1 (2008)
Herb Doctors archive

Politics & Science: Ray Peat on Biochemical Health, Oxidation, Reduction (2015)
Politics & Science: Evolution and Lamarck (2015)
Politics & Science: William Blake and more (2014)
Politics & Science: Call In Show (2013)
Politics & Science: Autoimmune and movement disorders (2012)
Politics & Science: Dogmatism in Science (2008)
Politics & Science: Origins of Life (2000)
Politics & Science: Suppression of Cancer Treatments – Dr. Ivy and Krebiozen (2001)
Politics & Science: Two Hour Fundraiser Part 1 (2012)
Politics & Science: Two Hour Fundraiser Part 2 (2012)
Politics & Science: Progesterone Part 1 (2012)
Politics & Science: Progesterone Part 2 (2012)
Politics & Science: Progesterone Part 3 (2012)
Politics & Science: Food Quality (2012)
Politics & Science: A Self Ordering World
Politics & Science: Fats
Politics & Science: Ionizing Radiation in Context, Parts 1 & 2
Politics & Science: Nuclear Disaster
Politics & Science: Obfuscation of Radiation Science by Industry
Politics & Science: Thyroid and Regeneration
Politics & Science: Machinist Scientist

One Radio Network: Dr. Ray Peat, Ph.D – Answering a Plethora of Questions Regarding Health, Diet and Nutrition Part 1 (2014)
One Radio Network: Dr. Ray Peat, Ph.D – Answering a Plethora of Questions Regarding Health, Diet and Nutrition Part 2 (2014)

Sharon Kleyne Hour Interview – Water (2013)

KWAI 1080 AM Interview 1 (2012)
KWAI 1080 AM Interview 2 (2012)

NPR Interview: The Thyroid (1996)

World Puja: Foundational Hormones

Hope for Health: Thyroid

Rainmaking Time: Life Supporting Substances
Rainmaking Time: Energy-Protective Materials (2014)

Eluv Interview: Effects of Stress and Trauma Part 1 (2014) [begins at 17:28]
Eluv Interview: Effects of Stress and Trauma Part 2 (2014)
Eluv Interview: Fats

East West – Energy and Metabolism (2013)
East West – Q&A Show 2
East West – Cholesterol and Saturated Fat
East West – Serotonin and Endotoxin
East West – Q&A Show
East West – Milk, Calcium, Hormones
East West – Glycemia, Starch, Sugar
East West – Estrogen, Progesterone
East West – Thyroid
East West – Inflammation
East West – Dangers of PUFA

The following are courtesy of Bud Weiss:
Bud Weiss Sept. 2008
Bud Weiss Audio Biology of Carbon Dioxide Oct. 2010
Bud Weiss Video Biology of Carbon Dioxide Oct. 2010

Posted in General.

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T3 Therapy to Reset Low Body Temperature in Hypothyroidism

Also see:
Wilson’s Temperature Syndrome
Basis Guidelines Wilson T3 Protocol
Wilson’s Temperature Tracking Chart
Wilson’s low Temperature Syndrome
Wilson Treatment Guidelines
Ray Peat, PhD on Thyroid, Temperature, Pulse, and TSH
Dosing with T3-only (or with low-dose NDT, or the combination of T4/T3)







Posted in General.

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Bodily Resources vs Demands

Also see:
Stress — A Shifting of Resources
Collection of FPS Charts
Sugar (Sucrose) Restrains the Stress Response
Low Blood Sugar Basics
Ray Peat, PhD on Low Blood Sugar & Stress Reaction
Bowel Toxins Accelerate Aging
Exercise Induced Stress
Carbohydrate Lowers Exercise Induced Stress
Low Carb Diet – Death to Metabolism
Can Endurance Sports Really Cause Harm? The Lipopolysaccharides of Endotoxemia and Their Effect on the Heart
Running on Empty
Exercise and Endotoxemia
Ray Peat, PhD on Endotoxin
Endotoxin: Poisoning from the Inside Out
Ray Peat, PhD: Quotes Relating to Exercise

“Life is a condition alternating between excitation, destruction and unbalance, and reorganization, equilibrium and rest.” -Kurt Goldstein

The bucket pictogram below, inspired the efforts of from James Clear, explains many health concepts. The body resources bucket contains some of the primary factors that ensure good health. These resources are drained by the body’s demands (dotted arrow), which vary from person to person.

Bodily Resources vs Demands

Bodily Resources vs Demands

The global objective is to maximize bodily resources and minimize demands to avoid momentary or permanent changes in bodily function. Tilt the scales in your favor.

Screen Shot 2016-08-01 at 7.56.30 PM

The body’s resources are finite, and the rate at which they are depleted is determined by your body’s demands. Maintain body balance by ensuring that your resources always trump your body’s demands by continually depositing resources on a daily basis and reducing demands where possible.

Young people are free of disease because their bodily resources are so vast that demands are easily met. When young people are compromised, they recover easily because they can quickly tilt the scales back in their favor.

There are direct parallels between finance and these two buckets. The resources bucket is analogous to a savings account, and the demands bucket represents total expenses. Don’t spend more money than you have to avoid financial turmoil or bankruptcy. Make deposits into your resources bucket on a daily basis and reduce expenses/demands to ensure protection from resource bankruptcy and a compromised body.

Here are some additional bullet points:

• The contents of each bucket will vary for each person. Some of the most basic elements are listed that apply to most people.
• Weight management and health concerns at their base come about due to imbalance between resources and demands. Each person has his/her own adaptation to the imbalance. Consider how robust your resources are at present and have been over your lifespan. Your present state is a reflection of all your years put together.
• Simple example of this pictogram at work is when one gets a cold or sickness. Someone gets a cold because demands were excessive relative to their (immune) resources. When someone gets a cold, he/she doesn’t go exercise vigorously (which is another demand) because energy levels and appetite are low. Rather, he/she builds lowers demands by taking time off from work/school if possible and sleeping/resting more and eventually eating well to build up his/her resources again to achieve recovery. If a person cannot aggregate the resources necessary to overcome the illness, the illness remains. How often you get sick and how long it takes you to recover when you do get sick is one indicator of how robust your resources bucket is.
• Restorative sleep and midday naps are an outstanding way to lower demands on your system.
• A person with sleep difficulties (sleep apnea, mouth breathing while sleeping, insomnia, waking several times during the night, waking feeling unrested, nocturnal urination, teeth grinding) is often the individual with high demands but low available resources. This creates a vicious cycle because of the inability to lower demands significantly via restorative sleep.

Additional Resources:
“The Stress of Life” by Hans Selye (book)
“Stress Without Distress” by Hans Selye (book)
“Why Zebras Don’t Get Ulcers” by Robert Sapolsky (book)
“Theory of Cumulative Stress – How to Recover When Stress Builds Up” by James Clear (online)

Posted in General.

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Calcium to Phosphorus Ratio of Vegetables and Fruits

Also see:
Calcium to Phosphorus Ratio, PTH, and Bone Health
Calcium to Phosphorus Ratio of Milk, Cheeses, Ice Cream by DrJ on RayPeatForum
Calcium Paradox
Source of Dietary Calcium: Chicken Egg Shell Powder
Low CO2 in Hypothyroidism
Blood Pressure Management with Calcium & Dairy
Hypertension and Calcium Deficiency
Excess Dietary Phosphorus Lowers Vitamin D Levels
Fatty Acid Synthase (FAS), Vitamin D, and Cancer
Phosphate, activation, and aging
Parmigiano Reggiano cheese and bone health
Preparing Powdered Eggshells for Calcium
Dairy, Calcium, and Weight Management in Adults and Children

Quotes by Ray Peat, PhD:
“The ratio of calcium to phosphate is very important; that’s why milk and cheese are so valuable for weight loss, or for preventing weight gain. For people who aren’t very active, low fat milk and cheese are better, because the extra fat calories aren’t needed.”

“The foods highest in phosphate, relative to calcium, are cereals, legumes, meats, and fish. Many prepared foods contain added phosphate. Foods with a higher, safe ratio of calcium to phosphate are leaves, such as kale, turnip greens, and beet greens, and many fruits, milk, and cheese.”

“Recent publication are showing that excess phosphate can increase inflammation, tissue atrophy, calcification of blood vessels, cancer, dementia, and, in general, the processes of aging.”

======================================================

This is a useful chart of fruits and vegetables ordered from highest to lowest calcium to phosphorus ratio (Ca:P). A ratio of 1.3:1 or higher is best to help keep parathyroid hormone down and protect cells from energy slowdowns and soft tissues from hardening/calcifying. The fruits and vegetables with a good ratio complement the consumption of milk and cheese.

Chart Source

GUINEA LYNX’ Sortable Veg & Fruit Chart
Pre-sorted to Ca:P
10 Calorie Quantities
Grams Sugar gm Calcium mg Ca:P Phos mg Magn mg Pot mg Sodium mg Vit_A RAE Vit_C mg
COLLARDS 33 0.15 48.33 14.5:1 3.33 3.00 56.33 6.67 111.00 11.77
BUTTERBUR,(FUKI) 71 UNKN 73.57 8.6:1 8.57 10.00 467.86 5.00 2.14 22.50
MUSTARD SPINACH,(TENDERGREEN) 45 UNKN 95.46 7.5:1 12.73 5.00 204.09 9.55 225.00 59.09
PAPAYAS 26 1.51 6.15 4.8:1 1.28 2.60 65.90 0.77 14.10 15.85
TURNIP GREENS 31 0.25 59.38 4.5:1 13.13 9.70 92.50 12.50 180.94 18.75
LAMBSQUARTERS 23 UNKN 71.86 4.3:1 16.74 7.90 105.12 10.00 134.88 18.61
DILL WEED,FRSH 23 UNKN 48.37 3.2:1 15.35 12.80 171.63 14.19 89.77 19.77
BASIL,FRESH 43 0.13 76.96 3.2:1 24.35 27.80 128.26 1.74 114.78 7.83
ARUGULA 40 0.82 64.00 3.1:1 20.80 18.80 147.60 10.80 47.60 6.00
ORANGES,ALL COMM VAR 21 1.99 8.51 2.9:1 2.98 2.10 38.51 UNKN 2.34 11.32
BEET GREENS 45 0.23 53.18 2.9:1 18.64 31.80 346.36 102.73 143.64 13.64
CABBAGE,CHINESE (PAK-CHOI) 77 0.91 80.77 2.8:1 28.46 14.60 193.85 50.00 171.54 34.62
DANDELION GREENS 22 0.16 41.56 2.8:1 14.67 8.00 88.22 16.89 112.89 7.78
CABBAGE,CHINESE (PE-TSAI) 63 0.88 48.13 2.7:1 18.13 8.10 148.75 5.63 10.00 16.88
KALE 20 UNKN 27.00 2.4:1 11.20 6.80 89.40 8.60 153.80 24.00
MUSTARD GREENS 38 0.62 39.62 2.4:1 16.54 12.30 136.15 9.62 201.92 26.92
PARSLEY 28 0.24 38.33 2.4:1 16.11 13.90 153.89 15.56 116.94 36.94
MELONS,CASABA 36 2.03 3.93 2.2:1 1.79 3.90 65.00 3.21 UNKN 7.79
NEW ZEALAND SPINACH 71 UNKN 41.43 2.1:1 20.00 27.90 92.86 92.86 157.14 21.43
WATERCRESS 91 0.18 109.09 2.0:1 54.55 19.10 300.00 37.27 145.46 39.09
SPINACH 43 0.18 43.04 2.0:1 21.30 34.40 242.61 34.35 203.91 12.22
SQUASH,WNTR,SPAGHETTI 32 UNKN 7.42 1.9:1 3.87 3.90 34.84 5.48 0.97 0.68
ENDIVE 59 0.15 30.59 1.9:1 16.47 8.80 184.71 12.94 63.53 3.82
TANGERINES,(MANDARIN ORANGES) 19 1.76 6.98 1.8:1 3.77 2.30 31.32 0.38 6.42 5.04
CELERY 63 1.14 25.00 1.7:1 15.00 6.90 162.50 50.00 13.75 1.94
PINEAPPLE,ALL VAR 20 1.97 2.60 1.6:1 1.60 2.40 21.80 0.20 0.60 9.56
PURSLANE 63 UNKN 40.63 1.5:1 27.50 42.50 308.75 28.13 41.25 13.13
ANISE SEED 3 UNKN 19.17 1.5:1 13.06 5.10 42.76 0.48 0.48 0.62
CABBAGE 40 1.28 16.00 1.5:1 10.40 4.80 68.00 7.20 2.00 14.64
CABBAGE,RED 32 1.24 14.52 1.5:1 9.68 5.20 78.39 8.71 18.07 18.39
SQUASH,WNTR,BUTTERNUT 22 0.49 10.67 1.5:1 7.33 7.60 78.22 0.89 118.22 4.67
BROCCOLI RAAB 45 0.17 49.09 1.5:1 33.18 10.00 89.09 15.00 59.55 9.18
CORIANDER (CILANTRO) LEAVES 43 0.38 29.13 1.4:1 20.87 11.30 226.52 20.00 146.52 11.74
RADISHES 63 1.16 15.63 1.3:1 12.50 6.30 145.63 24.38 UNKN 9.25
BLACKBERRIES 23 1.14 6.74 1.3:1 5.12 4.70 37.67 0.23 2.56 4.88
SQUASH,WNTR,ALL VAR 29 0.65 8.24 1.2:1 6.77 4.10 102.94 1.18 20.00 3.62
LETTUCE,GRN LEAF 67 0.52 24.00 1.2:1 19.33 8.70 129.33 18.67 246.67 12.00
LETTUCE,RED LEAF 63 0.30 20.63 1.2:1 17.50 7.50 116.88 15.63 234.38 2.31
CHERRIES,SOUR,RED 20 1.70 3.20 1.1:1 3.00 1.80 34.60 0.60 12.80 2.00
CRESS,GARDEN 31 1.38 25.31 1.1:1 23.75 11.90 189.38 4.38 108.13 21.56
TURNIPS 36 1.36 10.71 1.1:1 9.64 3.90 68.21 23.93 UNKN 7.50
CARROTS,BABY 29 1.36 9.14 1.1:1 8.00 2.90 67.71 22.29 197.14 0.74
LETTUCE,BUTTERHEAD (INCL BOSTON&BIBB TYPES) 77 0.72 26.92 1.1:1 25.39 10.00 183.08 3.85 127.69 2.85
LETTUCE,COS OR ROMAINE 59 0.70 19.41 1.1:1 17.65 8.20 145.29 4.71 256.47 14.12
CHARD,SWISS 53 0.58 26.84 1.1:1 24.21 42.60 199.47 112.11 161.05 15.79
KIWIFRUIT,GRN 16 1.47 5.57 1.0:1 5.57 2.80 51.15 0.49 0.66 15.20
BEANS,SNAP,GREEN 32 1.05 11.94 1.0:1 12.26 8.10 68.07 1.94 11.29 3.94
SQUASH,WINTER,ACORN 25 UNKN 8.25 0.9:1 9.00 8.00 86.75 0.75 4.50 2.75
MANGOS 15 2.28 1.54 0.9:1 1.69 1.40 24.00 0.31 5.85 4.26
LETTUCE,ICEBERG (INCL CRISPHEAD TYPES) 71 1.41 12.86 0.9:1 14.29 5.00 100.71 7.14 17.86 2.00
CARROTS 24 1.16 8.05 0.9:1 8.54 2.90 78.05 16.83 203.66 1.44
RASPBERRIES 19 0.85 4.81 0.9:1 5.58 4.20 29.04 0.19 0.39 5.04
SALSIFY,(VEG OYSTER) 12 UNKN 7.32 0.8:1 9.15 2.80 46.34 2.44 UNKN 0.98
PEARS 17 1.69 1.55 0.8:1 1.90 1.20 20.52 0.17 0.17 0.72
RUTABAGAS 28 1.56 13.06 0.8:1 16.11 6.40 93.61 5.56 UNKN 6.94
PEAS,EDIBLE-PODDED 24 0.95 10.24 0.8:1 12.62 5.70 47.62 0.95 12.86 14.29
CABBAGE,SAVOY 37 0.84 12.96 0.8:1 15.56 10.40 85.19 10.37 18.52 11.48
SQUASH,WINTER,HUBBARD 25 UNKN 3.50 0.7:1 5.25 4.80 80.00 1.75 17.00 2.75
SQUASH,SMMR,CROOKNECK&STRAIGHTNECK 53 1.86 11.05 0.7:1 16.84 10.50 116.84 1.05 4.21 10.16
STRAWBERRIES 31 1.53 5.00 0.7:1 7.50 4.10 47.81 0.31 0.31 18.38
CUCUMBER,WITH PEEL 67 1.11 10.67 0.7:1 16.00 8.70 98.00 1.33 3.33 1.87
BROCCOLI 29 0.50 13.82 0.7:1 19.41 6.20 92.94 9.71 9.12 26.24
MELONS,CANTALOUPE 29 2.31 2.65 0.6:1 4.41 3.50 78.53 4.71 49.71 10.79
WATERMELON 33 2.07 2.33 0.6:1 3.67 3.30 37.33 0.33 9.33 2.70
CHERRIES,SWEET 16 2.04 2.06 0.6:1 3.33 1.80 35.24 UNKN 0.48 1.11
CRANBERRIES 22 0.88 1.74 0.6:1 2.83 1.30 18.48 0.44 0.65 2.89
BRUSSELS SPROUTS 23 0.51 9.77 0.6:1 16.05 5.40 90.47 5.81 8.84 19.77
SWEET POTATO,UNPREP 12 0.49 3.49 0.6:1 5.47 2.90 39.19 6.40 82.44 0.28
RADISH SEEDS,SPROUTED 23 UNKN 11.86 0.5:1 26.28 10.20 20.00 1.40 4.65 6.72
SQUASH,SUMMER,SCALLOP 56 UNKN 10.56 0.5:1 20.00 12.80 101.11 0.56 3.33 10.00
PEPPERS,SWEET,YELLOW 37 UNKN 4.07 0.5:1 8.89 4.40 78.52 0.74 3.70 67.96
MELONS,HONEYDEW 28 2.26 1.67 0.5:1 3.06 2.80 63.33 5.00 0.83 5.00
GRAPES,RED OR GRN (EURO TYPE,SUCH AS THOMPSON SEEDLESS) 14 2.24 1.45 0.5:1 2.90 1.00 27.68 0.29 0.44 1.57
APPLES,WITH SKIN 19 2.00 1.15 0.5:1 2.12 1.00 20.58 0.19 0.58 0.89
RAISINS,SEEDLESS 3 1.98 1.67 0.5:1 3.38 1.10 25.05 0.37 UNKN 0.08
RAISINS,GOLDEN SEEDLESS 3 1.96 1.76 0.5:1 3.81 1.20 24.70 0.40 UNKN 0.11
BLUEBERRIES 18 1.75 1.05 0.5:1 2.11 1.10 13.51 0.18 0.53 1.70
PEPPERS,SWT,GRN 50 1.20 5.00 0.5:1 10.00 5.00 87.50 1.50 9.00 40.20
KOHLRABI 37 0.96 8.89 0.5:1 17.04 7.00 129.63 7.41 0.74 22.96
ASPARAGUS 50 0.94 12.00 0.5:1 26.00 7.00 101.00 1.00 19.00 2.80
CAULIFLOWER 40 0.76 8.80 0.5:1 17.60 6.00 119.60 12.00 UNKN 19.28
PARSNIPS 13 0.64 4.80 0.5:1 9.47 3.90 50.00 1.33 UNKN 2.27
PUMPKIN 38 0.52 8.08 0.5:1 16.92 4.60 130.77 0.39 141.92 3.46
RADICCHIO 43 0.26 8.26 0.5:1 17.39 5.70 131.30 9.57 0.44 3.48
ALFALFA SEEDS,SPROUTED 43 0.08 13.91 0.5:1 30.44 11.70 34.35 2.61 3.48 3.57
SWEET POTATO LEAVES 29 UNKN 10.57 0.4:1 26.86 17.40 148.00 2.57 14.57 3.14
PLUMS 22 2.16 1.30 0.4:1 3.48 1.50 34.13 UNKN 3.70 2.07
PEARS,ASIAN 24 1.68 0.95 0.4:1 2.62 1.90 28.81 UNKN UNKN 0.91
BEETS 23 1.57 3.72 0.4:1 9.30 5.40 75.58 18.14 0.47 1.14
SQUASH,SMMR,ZUCCHINI,INCL SKN 59 1.47 9.41 0.4:1 22.35 10.60 153.53 4.71 5.88 10.53
TOMATOES,RED,RIPE,YEAR RND AVERAGE 56 1.46 5.56 0.4:1 13.33 6.10 131.67 2.78 23.33 7.06
SQUASH,SMMR,ALL VAR 63 1.38 9.38 0.4:1 23.75 10.60 163.75 1.25 6.25 10.63
BEANS,FAVA,IN POD 11 UNKN 4.21 0.3:1 14.66 3.80 37.73 2.84 1.93 0.42
PEACHES 26 2.15 1.54 0.3:1 5.13 2.30 48.72 UNKN 4.10 1.69
PEPPERS,SWT,RED 32 1.36 2.26 0.3:1 8.39 3.90 68.07 1.29 50.65 41.19
YAM 8 0.04 1.44 0.3:1 4.66 1.80 69.15 0.76 0.59 1.45
SQUASH,ZUCCHINI,BABY 48 UNKN 10.00 0.2:1 44.29 15.70 218.57 1.43 11.91 16.24
PEAS,MATURE SEEDS,SPROUTED 8 UNKN 2.90 0.2:1 13.31 4.50 30.73 1.61 UNKN 0.84
NECTARINES 23 1.79 1.36 0.2:1 5.91 2.10 45.68 UNKN 3.86 1.23
BANANAS 11 1.37 0.56 0.2:1 2.47 3.00 40.23 0.11 0.34 0.98
PEAS,GREEN 12 0.70 3.09 0.2:1 13.33 4.10 30.12 0.62 4.69 4.94
LENTILS,SPROUTED 9 UNKN 2.36 0.1:1 16.32 3.50 30.38 1.04 0.19 1.56
OATS 3 UNKN 1.39 0.1:1 13.45 4.60 11.03 0.05 UNKN UNKN
WHEAT GERM,CRUDE 3 UNKN 1.08 0.0:1 23.39 6.60 24.78 0.33 UNKN UNKN
CORN,SWT,YEL 12 0.73 0.23 0.0:1 10.35 4.30 31.40 1.74 1.05 0.79
CEREALS RTE,WHEAT GERM,TSTD,PLN 3 0.20 1.18 0.0:1 30.00 8.40 24.79 0.11 0.13 0.16

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Scott Sonnon Intuflow Joint Mobility

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Low Estrogen Content in Milk

Also see:
Toxic Plant Estrogens
Calcium to Phosphorus Ratio, PTH, and Bone Health
Calcium Paradox
Source of Dietary Calcium: Chicken Egg Shell Powder
Low CO2 in Hypothyroidism
Blood Pressure Management with Calcium & Dairy
Hypertension and Calcium Deficiency
Excess Dietary Phosphorus Lowers Vitamin D Levels
Fatty Acid Synthase (FAS), Vitamin D, and Cancer
Phosphate, activation, and aging
Parmigiano Reggiano cheese and bone health
Preparing Powdered Eggshells for Calcium
Dairy, Calcium, and Weight Management in Adults and Children

Key thoughts:
1. Low estrogen concentrations in milk.
2. More dietary fat equates to more estrogen content.
3. Goat milk has less estrogen than cow’s milk although both are low.
4. A study reporting high estrogen content in milk should also measure progesterone levels.

==========

J Dairy Sci. 2010 Jun;93(6):2533-40. doi: 10.3168/jds.2009-2947.
Estrone and 17beta-estradiol concentrations in pasteurized-homogenized milk and commercial dairy products.
Pape-Zambito DA1, Roberts RF, Kensinger RS.
Some individuals fear that estrogens in dairy products may stimulate growth of estrogen-sensitive cancers in humans. The presence of estrone (E(1)) and 17beta-estradiol (E(2)) in raw whole cow’s milk has been demonstrated. The objectives of this study were to determine if pasteurization-homogenization affects E(2) concentration in milk and to quantify E(1) and E(2) concentrations in commercially available dairy products. The effects of pasteurization-homogenization were tested by collecting fresh raw milk, followed by pasteurization and homogenization at 1 of 2 homogenization pressures. All treated milks were tested for milk fat globule size, percentages of milk fat and solids, and E(2) concentrations. Estrone and E(2) were quantified from organic or conventional skim, 1%, 2%, and whole milks, as well as half-and-half, cream, and butter samples. Estrone and E(2) were quantified by RIA after organic solvent extractions and chromatography. Pasteurization-homogenization reduced fat globule size, but did not significantly affect E(2), milk fat, or milk solids concentrations. Estrone concentrations averaged 2.9, 4.2, 5.7, 7.9, 20.4, 54.1 pg/mL, and 118.9 pg/g in skim, 1%, 2%, and whole milks, half-and-half, cream, and butter samples, respectively. 17Beta-estradiol concentrations averaged 0.4, 0.6, 0.9, 1.1, 1.9, 6.0 pg/mL, and 15.8 pg/g in skim, 1%, 2%, whole milks, half-and-half, cream, and butter samples, respectively. The amount of fat in milk significantly affected E(1) and E(2) concentrations in milk. Organic and conventional dairy products did not have substantially different concentrations of E(1) and E(2). Compared with information cited in the literature, concentrations of E(1) and E(2) in bovine milk are small relative to endogenous production rates of E(1) and E(2) in humans.

J Dairy Sci. 2007 Jul;90(7):3308-13.
Concentrations of 17beta-estradiol in Holstein whole milk.
Pape-Zambito DA1, Magliaro AL, Kensinger RS.
Some individuals have expressed concern about estrogens in food because of their potential to promote growth of estrogen-sensitive human cancer cells. Researchers have reported concentrations of estrogen in milk but few whole milk samples have been analyzed. Because estrogen associates with the fat phase of milk, the analysis of whole milk is an important consideration. The objectives of this study, therefore, were to quantify 17beta-estradiol (E2) in whole milk from dairy cows and to determine whether E2 concentrations in milk from cows in the second half of pregnancy were greater than that in milk from cows in the first half of pregnancy or in nonpregnant cows. Milk samples and weights were collected during a single morning milking from 206 Holstein cows. Triplicate samples were collected and 2 samples were analyzed for fat, protein, lactose, and somatic cell counts (SCC); 1 sample was homogenized and analyzed for E2. The homogenized whole milk (3 mL) was extracted twice with ethyl acetate and once with methanol. The extract was reconstituted in benzene:methanol (9:1, vol/vol) and run over a Sephadex LH-20 column to separate E2 from cholesterol and estrone before quantification using radioimmunoassay. Cows were classified as not pregnant (NP, n = 138), early pregnant (EP, 1 to 140 d pregnant, n = 47), or midpregnant (MP, 141 to 210 d pregnant, n = 21) at the time of milk sampling based on herd health records. Mean E2 concentration in whole milk was 1.4 +/- 0.2 pg/mL and ranged from nondetectable to 22.9 pg/mL. Milk E2 concentrations averaged 1.3, 0.9, and 3.0 pg/mL for NP, EP, and MP cows, respectively. Milk E2 concentrations for MP cows were greater and differed from those of NP and EP cows. Milk composition was normal for a Holstein herd in that log SCC values and percentages of fat, protein, and lactose averaged 4.9, 3.5, 3.1, and 4.8, respectively. Estradiol concentration was significantly correlated (r = 0.20) with percentage fat in milk. Mean milk yield was 18.9 +/- 0.6 kg for the morning milking. The mean E2 mass accumulated in the morning milk was 23.2 +/- 3.4 ng/cow. Likewise, using the overall mean concentration for E2 in milk, the mean E2 mass in 237 mL (8 fluid ounces) of raw whole milk was 330 pg. The quantity of E2 in whole milk, therefore, is low and is unlikely to pose a health risk for humans.

J Dairy Sci. 1979 Sep;62(9):1458-63.
Measurement of estrogens in cow’s milk, human milk, and dairy products.
Wolford ST, Argoudelis CJ.
Free natural estrogens in raw and commercial whole milk were quantitated by radioimmunoassay. The ranges of concentration of estrone, estradiol 17-beta, and estriol were 34 to 55, 4 to 14, and 9 to 31 pg/ml. Proportions of active estrogens (estrone and estradiol) in the fat phases of milk by radioactive tracer on separated milk were 80% and 65%. These findings were supported by radioimmunoassay of skim milk and butter. Equilibrium dialysis of skim milk with hydrogen 3 labeled estrogens showed that 84 to 85% of estrone and estradiol and 61 to 66% of estriol were protein bound. Whey proteins demonstrated a greater binding capacity than casein. This result was confirmed by radioimmunoassay of dry curd cottage cheese and whey. The concentrations in curd were 35, 11, and 6 pg/g. In whey they were 4, 2, and 3 pg/ml. The quantity of active estrogens in dairy products is too low to demonstrate biological activity. Butter was highest with concentrations of 539, 82, and 87 pg/g. Human colostrum demonstrated a maximum concentration of 4 to 5 ng/ml for estrone and estriol and about .5 ng/ml for estradiol. By the 5th day postpartum, they decreased to become similar to cow’s milk.

J Dairy Sci. 2012 Apr;95(4):1699-708. doi: 10.3168/jds.2011-5072.
Comparison of estrone and 17β-estradiol levels in commercial goat and cow milk.
Farlow DW1, Xu X, Veenstra TD.
Increased levels of estrogen metabolites are believed to be associated with cancers of the reproductive system. One potential dietary source of these metabolites that is commonly consumed worldwide is milk. In North America, dairy cows are the most common source of milk; however, goats are the primary source of milk worldwide. In this study, the absolute concentrations of unconjugated and total (unconjugated plus conjugated) estrone (E(1)) and 17β-estradiol (E(2)) were compared in a variety of commercial cow milks (regular and organic) and goat milk. A lower combined concentration of E(1) and E(2) was found in goat milk than in any of the cow milk products tested. The differences in E(1) and E(2) levels between regular and organic cow milks were not as significant as the differences between goat milk and any of the cow milk products. Goat milk represents a better dietary choice for individuals concerned with limiting their estrogen intake.

Iran J Public Health. 2015 Jun; 44(6): 742–758
Hormones in Dairy Foods and Their Impact on Public Health – A Narrative Review Article
Hassan MALEKINEJAD and Aysa REZABAKHSH

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NuSI Hall Study: No Ketogenic Advantage

Also See:
Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets.
Blood ketones are directly related to fatigue and perceived effort during exercise in overweight adults adhering to low-carbohydrate diets for weight loss: a pilot study.
PUFA, Ketones, and Sugar Restriction Promote Tumor Growth
Tumor Bearing Organisms – Lipolysis and Ketogenesis as Signs of Chronic Stress
Free Fatty Acids Suppress Cellular Respiration
The Randle Cycle
Ray Peat, PhD on Low Blood Sugar & Stress Reaction

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Polyunsaturating America: Mazola’s Marketing

Also see:
PUFA Promote Cancer
Unsaturated Fats and Heart Damage
Gelatin Ads
Sugar Ads
Errors in Nutrition: Essential Fatty Acids
Toxicity of Stored PUFA
Dietary PUFA Reflected in Human Subcutaneous Fat Tissue
PUFA Accumulation & Aging
Maternal PUFA Intake Increases Breast Cancer Risk in Female Offspring
Israeli Paradox: High Omega -6 Diet Promotes Disease
Benefits of Aspirin
Arachidonic Acid’s Role in Stress and Shock
Charts: Mean SFA, MUFA, & PUFA Content of Various Dietary Fats
Unsaturated fatty acids: Nutritionally essential, or toxic? by Ray Peat, PhD
“Curing” a High Metabolic Rate with Unsaturated Fats
Fat Deficient Animals – Activity of Cytochrome Oxidase
Anti-Inflammatory Omega -9 Mead Acid (Eicosapentaenoic acid)
Protective “Essential Fatty Acid Deficiency”
Cholesterol and Thyroid Connection
Thyroid Status and Cardiovascular Disease

A few factors collide starting in the 1970s to further expedite a departure from traditional animal fats towards polyunsaturated plant oils:

  • US government, under Nixon, subsidizes corn (corn oil/Mazola). Government later subsidizes soy and wheat.
  • Cheaper vegetable and seed (liquid) oils progressively replace animal fats, capitalizing on the ridiculous anti-cholesterol campaign and faulty lipid hypothesis.
  • Nutritional information from the government supports American industry, not health.

Mazola’s marketing campaign in the 1970s put polyunsaturated fats front and center in the American vernacular and placed saturated fats firmly as the bad guy. The marketing encouraged women to “polyunsaturate” their loved ones while avoiding saturates; in retrospect, this is the exact opposite of what is desired.

Over 40 years later, the US is still suffering from the ubiquitous use of vegetable oils. While milk, sugar, fructose, salt, and saturated fat take a beating from American society as nutritional toxins, polyunsaturated fats in their various forms continue to get a free pass. Evidence from Ray Peat, PhD and the FPS blog will hopefully help people come to their senses.

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Vitamin E Needs Increases with PUFA Consumption and Greater Unsaturation

Also See:
Your MUFA + PUFA Intakes Determine Your True Vitamin E Requirements – N-3s are the Worst Offenders + Even MUFAs Need Buffering | Tool to Calculate Your Individual NeedsVitamin E and Autoimmune Disease
Autoimmune Disease and Estrogen Connection
Dietary PUFA Reflected in Human Subcutaneous Fat Tissue
Toxicity of Stored PUFA
Israeli Paradox: High Omega -6 Diet Promotes Disease
PUFA Accumulation & Aging
Protective “Essential Fatty Acid Deficiency”
PUFA Promote Stress Response; Saturated Fats Suppress Stress Response
PUFA, Fish Oil, and Alzheimers

Int J Vitam Nutr Res. 2000 Mar;70(2):31-42.
Relationship between vitamin E requirement and polyunsaturated fatty acid intake in man: a review.
Valk EE1, Hornstra G.
Vitamin E is the general term for all tocopherols and tocotrienols, of which alpha-tocopherol is the natural and biologically most active form. Although gamma-tocopherol makes a significant contribution to the vitamin E CONTENT in foods, it is less effective in animal and human tissues, where alpha-tocopherol is the most effective chain-breaking lipid-soluble antioxidant. The antioxidant function of vitamin E is critical for the prevention of oxidation of tissue PUFA. Animal experiments have shown that increasing the degree of dietary fatty acid unsaturation increases the peroxidizability of the lipids and reduces the time required to develop symptoms of vitamin E deficiency. From these experiments, relative amounts of vitamin E required to protect the various fatty acids from being peroxidized, could be estimated. Since systematic studies on the vitamin E requirement in relation to PUFA consumption have not been performed in man, recommendations for vitamin E intake are based on animal experiments and human food intake data. An intake of 0.6 mg alpha-tocopherol equivalents per gram linoleic acid is generally seen as adequate for human adults. The minimum vitamin E requirement at consumption of fatty acids with a higher degree of unsaturation can be calculated by a formula, which takes into account the peroxidizability of unsaturated fatty acids and is based on the results of animal experiments. There are, however, no clear data on the vitamin E requirement of humans consuming the more unsaturated fatty acids as for instance EPA (20:5, n-3) and DHA (22:6, n-3). Studies investigating the effects of EPA and DHA supplementation have shown an increase in lipid peroxidation, although amounts of vitamin E were present that are considered adequate in relation to the calculated oxidative potential of these fatty acids. Furthermore, a calculation of the vitamin E requirement, using recent nutritional intake data, shows that a reduction in total fat intake with a concomitant increase in PUFA consumption, including EPA and DHA, will result in an increased amount of vitamin E required. In addition, the methods used in previous studies investigating vitamin E requirement and PUFA consumption (for instance erythrocyte hemolysis), and the techniques used to assess lipid peroxidation (e.g. MDA analysis), may be unsuitable to establish a quantitative relation between vitamin E intake and consumption of highly unsaturated fatty acids. Therefore, further studies are required to establish the vitamin E requirement when the intake of longer-chain, more-unsaturated fatty acids is increased. For this purpose it is necessary to use functional techniques based on the measurement of lipid peroxidation in vivo. Until these data are available, the widely used ratio of at least 0.6 mg alpha-TE/g PUFA is suggested. Higher levels may be necessary, however, for fats that are rich in fatty acids containing more than two double bonds.

Br J Nutr. 2015 Oct 28;114(8):1113-22. doi: 10.1017/S000711451500272X. Epub 2015 Aug 21.
Vitamin E function and requirements in relation to PUFA.
Raederstorff D1, Wyss A1, Calder PC2, Weber P1, Eggersdorfer M1.
Vitamin E (α-tocopherol) is recognised as a key essential lipophilic antioxidant in humans protecting lipoproteins, PUFA, cellular and intra-cellular membranes from damage. The aim of this review was to evaluate the relevant published data about vitamin E requirements in relation to dietary PUFA intake. Evidence in animals and humans indicates a minimal basal requirement of 4-5 mg/d of RRR-α-tocopherol when the diet is very low in PUFA. The vitamin E requirement will increase with an increase in PUFA consumption and with the degree of unsaturation of the PUFA in the diet. The vitamin E requirement related to dietary linoleic acid, which is globally the major dietary PUFA in humans, was calculated to be 0·4-0·6 mg of RRR-α-tocopherol/g of linoleic acid. Animal studies show that for fatty acids with a higher degree of unsaturation, the vitamin E requirement increases almost linearly with the degree of unsaturation of the PUFA in the relative ratios of 0·3, 2, 3, 4, 5 and 6 for mono-, di-, tri-, tetra-, penta- and hexaenoic fatty acids, respectively. Assuming a typical intake of dietary PUFA, a vitamin E requirement ranging from 12 to 20 mg of RRR-α-tocopherol/d can be calculated. A number of guidelines recommend to increase PUFA intake as they have well-established health benefits. It will be prudent to assure an adequate vitamin E intake to match the increased PUFA intake, especially as vitamin E intake is already below recommendations in many populations worldwide.

Z Ernahrungswiss. 1991 Sep;30(3):174-80.
On the problematic nature of vitamin E requirements: net vitamin E.
Bässler KH1.
The requirement for vitamin E is closely related to the dietary intake of polyunsaturated fatty acids (PUFA). By the protective mechanism to prevent PUFA from being peroxidized, vitamin E is metabolically consumed. In addition, PUFA impair the intestinal absorption of vitamin E. Therefore PUFA generate an additional vitamin E requirement on the order of 0.6, 0.9, 1.2, 1.5, and 1.8 mg vitamin E (RRR-alpha-tocopherol-equivalents), respectively, for 1 g of dienoic, trienoic, tetraenoic, pentaenoic, and hexaenoic acid. For this reason, the gross vitamin E content of food containing PUFA does not allow an evaluation of this food as a source of vitamin E. A suitable measure is the net vitamin E content, i.e., gross vitamin E minus the amount needed for PUFA protection. Therefore, some food-stuffs generally considered as vitamin-E sources, as concluded from their gross vitamin E content, cause in reality a vitamin E deficiency if not sufficiently compensated by other vitamin E supplying food constituents. Examples of the net vitamin E content of some fats and oils, fish and nuts are shown. Consequences for food composition data and food labeling and the problem of meeting the vitamin-E requirements are discussed.

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VIDEO: Are Happy Gut Bacteria Key to Weight Loss?

Also See:
Endotoxin: Poisoning from the Inside Out
Ray Peat, PhD on Endotoxin
Thumbs Up Fructose
Protective Effects of Citrus Flavanoid Naringenin
Bowel Toxins Accelerate Aging
Ray Peat, PhD on the Benefits of the Raw Carrot
Protection from Endotoxin
Endotoxin-lipoprotein Hypothesis
Protective Bamboo Shoots
The effect of raw carrot on serum lipids and colon function

Source

A few years before Super Size Me hit theaters in 2004, Dr. Paresh Dandona, a diabetes specialist in Buffalo, New York, set out to measure the body’s response to McDonald’s—specifically breakfast. Over several mornings, he fed nine normal-weight volunteers an egg sandwich with cheese and ham, a sausage muffin sandwich, and two hash brown patties.

Dandona is a professor at the State University of New York-Buffalo who also heads the Diabetes-Endocrinology Center of Western New York, and what he observed has informed his research ever since. Levels of a C-reactive protein, an indicator of systemic inflammation, shot up “within literally minutes.” “I was shocked,” he recalls, that “a simple McDonald’s meal that seems harmless enough”—the sort of high-fat, high-carbohydrate meal that 1 in 4 Americans eats regularly—would have such a dramatic effect. And it lasted for hours.

Inflammation comes in many forms. The swelling of a sprained ankle indicates repairing torn muscle and tendon. The redness and pain around an infected cut signifies the body’s repulsion of microbes. The fever, aches, and pains that accompany the flu represent a body-wide seek-and-destroy mission directed against an invading virus. They’re all essential to survival, the body’s response to a perceived threat or injury. But inflammation can also cause collateral damage, especially when the response is overwhelming—like in septic shock—or when it goes on too long.

Chronic, low-grade inflammation has long been recognized as a feature of metabolic syndrome, a cluster of dysfunctions that tends to precede full-blown diabetes and that also increases the risk of heart disease, stroke, certain cancers, and even dementia—the top killers of the developed world. The syndrome includes a combination of elevated blood sugar and high blood pressure, low “good” cholesterol, and an abdominal cavity filled with fat, often indicated by a “beer belly.” But recently, doctors have begun to question whether chronic inflammation is more than just a symptom of metabolic syndrome: Could it, in fact, be a major cause?

For Dandona, who’s given to waxing grandiloquent about the joys of a beer on the porch in his native Delhi, or the superb ice wines from the Buffalo region, the results presented a quandary. Food was a great pleasure in life. Why would Nature be so cruel, he wondered, and punish us just for eating?

Over the next decade he tested the effects of various foods on the immune system. A fast-food breakfast inflamed, he found, but a high-fiber breakfast with lots of fruit did not. A breakthrough came in 2007 when he discovered that while sugar water, a stand-in for soda, caused inflammation, orange juice—even though it contains plenty of sugar—didn’t.

The Florida Department of Citrus, a state agency, was so excited it underwrote a subsequent study, and had fresh-squeezed orange juice flown in for it. This time, along with their two-sandwich, two-hash-brown, 910-calorie breakfast, one-third of his volunteers—10 in total—quaffed a glass of fresh OJ. The non-juice drinkers, half of whom drank sugar water, and the other half plain water, had the expected response—inflammation and elevated blood sugar. But the OJ drinkers had neither elevated blood sugar nor inflammation. The juice seemed to shield their metabolism. “It just switched off the whole damn thing,” Dandona says. Other scientists have since confirmed that OJ has a strong anti-inflammatory effect.

Orange juice is rich in antioxidants like vitamin C, beneficial flavonoids, and small amounts of fiber, all of which may be directly anti-inflammatory. But what caught Dandona’s attention was another substance. Those subjects who ate just the McDonald’s breakfast had increased blood levels of a molecule called endotoxin. This molecule comes from the outer walls of certain bacteria. If endotoxin levels rise, our immune system perceives a threat and responds with inflammation.

If theories about the interplay of food and intestinal microbes pan out, it could help cure obesity and revolutionize the $66 billion weight loss industry.

Where had the endotoxin come from? One possibility was the food itself. But there was another possibility. We all carry a few pounds’ worth of microbes in our gut, a complex ecosystem collectively called the microbiota. The endotoxin, Dandona suspected, originated in this native colony of microbes. Somehow, a greasy meal full of refined carbohydrates ushered it from the gut, where it was always present but didn’t necessarily cause harm, into the bloodstream, where it did. But orange juice stopped that translocation cold.

Dandona’s ongoing experiments—and others like it—could upend much of we thought we knew about the causes of obesity, or just that extra pesky 10 pounds of flab. If what some scientists now suspect about the interplay of food and intestinal microbes pans out, it could revolutionize the $66 billion weight loss industry—and help control the soaring $2.7 trillion we spend on health care yearly. “What matters is not how much you eat,” Dandona says, “but what you eat.”
EVER SINCE THE DUTCH DRAPER Antonie van Leeuwenhoek first scrutinized his own plaque with a homemade microscope more than three centuries ago and discovered “little living animalcules, very prettily a-moving,” we’ve known that we’re covered in microbes. But as new and cheaper methods for studying these microbes have become available recently, their importance to our health has grown increasingly evident. Scientists now suspect that our microbial communities contribute to a number of diseases, from allergic disorders like asthma and hay fever, to inflammatory conditions like Crohn’s disease, to cancer, heart disease, and obesity.

We are, numerically speaking, 10 percent human, and 90 percent microbe.

As newborns, we encounter our first microbes as we pass through the birth canal. Until that moment, we are 100 percent human. Thereafter, we are, numerically speaking, 10 percent human, and 90 percent microbe. Our microbiome contains at least 150 times more genes, collectively, than our human genome. Think of it as a hulking instruction manual compared to a single page to-do list.

As we mature, we pick up more microbes from breast milk, food, water, animals, soil, and other people. Sometime in childhood, the bustling community of between 500 and 1,000 species stabilizes. Some species are native only to humans, and may have been passed down within the family like heirlooms. Others are generalists—maybe they’ve hopped aboard from pets, livestock, and other animal sources.

Enterobacter cloacae

A cluster of Enterobacter cloacae bacteria Eye of Science / Science Source

Most of our microbes inhabit the colon, the final loop of intestine, where they help us break down fibers, harvest calories, and protect us from micro-marauders. But they also do much, much more. Animals raised without microbes essentially lack a functioning immune system. Entire repertoires of white blood cells remain dormant; their intestines don’t develop the proper creases and crypts; their hearts are shrunken; genes in the brain that should be in the “off” position remain stuck “on.” Without their microbes, animals aren’t really “normal.”

What do we do for our microbes in return? Some scientists argue that mammals are really just mobile digestion chambers for bacteria. After all, your stool is roughly half living bacteria by weight. Every day, food goes in one end and microbes come out the other. The human gut is roughly 26 feet in length. Hammered flat, it would have a surface area of a tennis court. Seventy percent of our immune activity occurs there. The gut has its own nervous system; it contains as many neurons as the spinal cord. About 95 percent of the body’s serotonin, a neurotransmitter usually discussed in the context of depression, is produced in the gut.

Children raised in microbially rich environments—with pets, on farms, or attending day care—are at lower risk of allergic diseases.

So the gut isn’t just where we absorb nutrients. It’s also an immune hub and a second brain. And it’s crawling with microbes. They don’t often cross the walls of the intestines into the blood stream, but they nevertheless change how the immune, endocrine, and nervous systems all work on the other side of the intestine wall.

Science isn’t always consistent about what, exactly, goes wrong with our microbes in disease situations. But a recurrent theme is that loss of diversity correlates with the emergence of illness. Children in the developing world have many more types of microbes than kids in Europe or North America, and yet generally develop allergies and asthma at lower rates than those in industrialized nations. In the developed world, children raised in microbially rich environments—with pets, on farms, or attending day care—have a lower risk of allergic disease than kids raised in more sterile environments.

metabolism flowchart

Those who study human microbial communities fret that they are undergoing an extinction crisis similar to the one afflicting the biosphere at large—and that modern medicine may be partly to blame. Some studies find that babies born by C-section, deprived of their mother’s vaginal microbes at birth, have a higher risk of celiac disease, Type 1 diabetes, and obesity. Early-life use of antibiotics—which tear through our microbial ecosystems like a forest fire—has also been linked to allergic disease, inflammatory bowel disease, and obesity.

Which brings us to the question more and more scientists are asking: If our microbiota plays a role in keeping us healthy, then how about attacking disease by treating the microbiota? After all, our community of microbes is quite plastic. New members can arrive and take up residence. Old members can get flushed out. Member ratios can shift. The human genome, meanwhile, is comparatively stiff and unresponsive. So the microbiota represents a huge potential leverage point in our quest to treat, and prevent, chronic disease. In particular, the “forgotten organ,” as some call the microbiota, may hold the key to addressing our single greatest health threat: obesity.
PARESH DANDONA LEFT INDIA in 1966 for a Rhodes Scholarship at Oxford University. He became “the first colored guy,” he says, to head his unit at the University of London hospital. His bearing—heels together, back stiff, and an orator’s care with words delivered in a deep, sonorous voice—recalls a bygone era. He moved to Buffalo in 1991.

During those decades, the number of Americans considered obese nearly tripled. One-third of Americans are now considered overweight, and another third obese. Worldwide, one-fourth of humanity is too heavy, according to the World Health Organization. In 2011, the United Nations announced that for the first time ever, chronic diseases, most of which are linked to obesity, killed more people than infectious diseases. In the United States, obesity accounts for 20 percent of health care costs, according to Cornell University economists.

And the problems aren’t limited to the obese themselves: Children born to obese mothers have hardened arteries at birth, a risk factor for cardiovascular disease. They have a greater risk of asthma. Some studies suggest they’re more likely to suffer from attention deficit disorders and autism.

Why are we increasingly prone to obesity? The long-dominant explanation is simply that too little exercise and too many calories equals too much stored fat. The solution: more exercise and a lot more willpower. But there’s a problem with this theory: In the developed world, most of us consume more calories than we really need, but we don’t gain weight proportionally.

A pound of body fat contains roughly 3,500 calories. If you run a daily surplus of just 500 calories—the amount in a bagel with a generous serving of cream cheese—you should, judging by the strict calorie-in-must-equal-calorie-out model, gain a pound of fat per week. Most of us do run a surplus in that range, or even higher, but we either gain weight much more slowly, or don’t gain weight at all.

Some corpulent people, meanwhile, have metabolisms that work fine. Their insulin and blood sugar levels are within normal range. Their livers are healthy, not marbled with fat. And some thin people have metabolic syndrome, often signaled by a beer gut. They suffer from fatty liver, insulin resistance, elevated blood sugar, high blood pressure, and low-grade, systemic inflammation. From a public health perspective, these symptoms are where the real problem lies—not necessarily how well we fit into our jeans.

Inflammation might not be a symptom of metabolic syndrome: It could be a cause.

Here’s the traditional understanding of metabolic syndrome: You ate too much refined food sopped in grease. Calories flooded your body. Usually, a hormone called insulin would help your cells absorb these calories for use. But the sheer overabundance of energy in this case overwhelms your cells. They stop responding to insulin. To compensate, your pancreas begins cranking out more insulin. When the pancreas finally collapses from exhaustion, you have diabetes. In addition, you develop resistance to another hormone called leptin, which signals satiety, or fullness. So you tend to overeat. Meanwhile, fat cells, which have become bloated and stressed as they try to store the excess calories, begin emitting a danger signal—low-grade inflammation.

But new research suggest another scenario: Inflammation might not be a symptom, it could be a cause. According to this theory, it is the immune activation caused by lousy food that prompts insulin and leptin resistance. Sugar builds up in your blood. Insulin increases. Your liver and pancreas strain to keep up. All because the loudly blaring danger signal—the inflammation—hampers your cells’ ability to respond to hormonal signals. Maybe the most dramatic evidence in support of this idea comes from experiments where scientists quash inflammation in animals. If you simply increase the number of white blood cells that alleviate inflammation—called regulatory T-cells—in obese mice with metabolic syndrome, the whole syndrome fades away. Deal with the inflammation, it seems, and you halt the dysfunction.

Now, on the face of it, it seems odd that a little inflammation should have such a great impact on energy regulation. But consider: This is about apportioning a limited resource exactly where it’s needed, when it’s needed. When not under threat, the body uses energy for housekeeping and maintenance—and, if you’re lucky, procreation, an optimistic, future-oriented activity. But when a threat arrives—a measles virus, say—you reprioritize. All that hormone-regulated activity declines to a bare minimum. Your body institutes a version of World War II rationing: troops (white blood cells) and resources (calories) are redirected toward the threat. Nonessential tasks, including the production of testosterone, shut down. Forget tomorrow. The priority is to preserve the self today.

This, some think, is the evolutionary reason for insulin resistance. Cells in the body stop absorbing sugar because the fuel is required—requisitioned, really—by armies of white blood cells. The problems arise when that emergency response, crucial to repelling pillagers in the short term, drags on indefinitely. Imagine it this way. Your dinner is cooking on the stove. You’re paying bills. You smell smoke. You jump up, leaving those tasks half-done, and search for the fire before it burns down your house. Normally, once you put the fire out, you’d return to your tasks and then eat dinner.

Junk food may not kill us directly, but rather by prompting the collapse of an ancient and mutually beneficial symbiosis.

But now imagine that you never find the fire, and you never stop smelling the smoke. You remain in a perpetual state of alarm. Your bills never get paid. You never eat your dinner. Your house smolders. Your life falls into disarray.

That’s metabolic syndrome. Normal function ceases. Aging accelerates. Diabetes develops. Heart attacks strike. The brain degenerates. Life ends early. And it’s all driven, in this understanding, by chronic, low-grade inflammation.

Where does the perceived threat come from—all that inflammation? Some ingested fats are directly inflammatory. And dumping a huge amount of calories into the bloodstream from any source, be it fat or sugar, may overwhelm and inflame cells. But another source of inflammation is hidden in plain sight, the 100 trillion microbes inhabiting your gut. Junk food, it turns out, may not kill us entirely directly, but rather by prompting the collapse of an ancient and mutually beneficial symbiosis, and turning a once cooperative relationship adversarial.

We’re already familiar with a version of this dynamic: cavities. Tooth decay is as old as teeth, but it intensified with increased consumption of refined carbohydrates, like sugar, just before and during the industrial revolution. Before cheap sugar became widely available, plaque microbes probably occupied the warm and inviting ecological niche of your mouth more peaceably. But dump a load of sugar on them, and certain species expand exponentially. Their by-product—acid—which, in normal amounts, protects you from foreign bacteria—now corrodes your teeth. A once cooperative relationship becomes antagonistic.

Something similar may occur with our gut microbes when they’re exposed to the highly refined, sweet, and greasy junk-food diet. They may turn against us.
A DECADE AGO, microbiologists at Washington University in St. Louis noticed that mice raised without any microbes, in plastic bubbles with positive air pressure, could gorge on food without developing metabolic syndrome or growing obese. But when colonized with their native microbes, these mice quickly became insulin resistant and grew fat, all while eating less food than their germ-free counterparts.

The researchers surmised that the microbes helped the rodents harvest energy from food. The mice, which then had more calories than they needed, stored the surplus as fat. But across the Atlantic, Patrice Cani at the Catholic University of Louvain in Brussels, Belgium, suspected that inflammation contributed, and that the inflammation emanated from native microbes.

To prove the principle, he gave mice a low dose of endotoxin, that molecule that resides in the outer walls of certain bacteria. The mice’s livers became insulin resistant; the mice became obese and developed diabetes. A high-fat diet alone produced the same result: Endotoxin leaked into circulation; inflammation took hold; the mice grew fat and diabetic. Then came the bombshell. The mere addition of soluble plant fibers called oligosaccharides, found in things like bananas, garlic, and asparagus, prevented the entire cascade—no endotoxin, no inflammation, and no diabetes.

“If we take care of our gut microbiota, it will take care of our health,” says one researcher. “I like to finish my talks with one sentence: ‘In gut we trust.'”

Oligosaccharides are one form of what’s known as a “prebiotic”: fibers that, because they make it all the way to the colon intact, feed, as it were, the bacteria that live there. One reason we’ve evolved to house microbes at all is because they “digest” these fibers by fermenting them, breaking them down and allowing us to utilize their healthful byproducts, like acetic acid, butyric acid, B vitamins, and vitamin K.

Cani had essentially arrived at the same place as Dandona with his freshly squeezed orange juice. Only his controlled animal experiments allowed a clearer understanding of the mechanisms. Junk food caused nasty microbes to bloom, and friendly bugs to decline. Permeability of the gut also increased, meaning that microbial byproducts—like that endotoxin—could more easily leak into circulation, and spur inflammation. Simply adding prebiotics enjoyed by a select group of microbes—in this case, Bifidobacteria—kept the gut tightly sealed, preventing the entire cascade. The fortified bacteria acted like crowd-control police, keeping the rest of the microbial mob from storming the barrier.

“If we take care of our gut microbiota, it will take care of our health,” Cani says. “I like to finish my talks with one sentence: ‘In gut we trust.'”

So our sweet and greasy diet—almost certainly without evolutionary precedent—doesn’t just kill us directly: It also changes gut permeability and alters the makeup of our microbial organ. Our “friendly” community of microbes becomes unfriendly, even downright pathogenic, leaking noxious byproducts where they don’t belong. H.G. Wells would be proud of this story—the mighty Homo sapiens felled by microscopic life turned toxic by junk food. It’s nothing personal; the bugs that bloom with an energy-dense diet may act in their own self-interest. They want more of that food sweet, fatty food on which they thrive.
AROUND THE TIME when Paresh Dandona began puzzling over the immune response to a fast-food breakfast, a Chinese microbiologist named Liping Zhao was realizing that he needed to change how he ate, or he might drop dead. He was 44 pounds overweight, his blood pressure was elevated, and his “bad” cholesterol was high.

He caught wind of the studies at Washington University in St. Louis suggesting that microbes were central to obesity. The research jibed with ancient precepts in Chinese medicine that viewed the gut as central to health. So Zhao decided on a hybridized approach—some 21st-century microbiology topped with traditional Chinese medicine.

He changed his diet to whole grains, rich in those prebiotic fibers important for beneficial bacteria. And he began regularly consuming two traditional medicinal foods thought to have such properties: bitter melon and Chinese yam.

Zhao’s blood pressure began normalizing and his “bad” cholesterol declined. Over the course of two years, he lost 44 pounds. He sampled his microbes throughout. As his metabolism normalized, quantities of a bacterium called Faecalibacterium prausnitzii increased in his gut. Was its appearance cause or consequence? Others have observed that this bacterium is absent in people suffering from inflammatory diseases, such as Crohn’s disease, as well as Type 2 diabetes. Scientists at the University of Tokyo have shown that colonizing mice with this bacterium and its relatives—called “Clostridium clusters”—protects them against colitis. But still, evidence of causation was lacking.

Then one day in 2008, a morbidly obese man walked into Zhao’s lab in China. The 26-year-old was diabetic, inflamed, had high bad cholesterol, and elevated blood sugar. No one in his immediate family was heavy, but he weighed 385 pounds.

Aided by a high fat diet, the microbe appeared able to hijack the metabolism of both mice and man.

Zhao noticed something odd about the man’s microbes. Thirty-five percent belonged to a single, endotoxin-producing species called Enterobacter cloacae. So he put the man on a version of his own regimen—whole grains supplemented with other prebiotics. As treatment progressed, the Enterobacter cloacae declined, as did circulating endotoxin and markers of inflammation.

After 23 weeks, the man had lost 113 pounds. That bacterial bloom had receded to the point of being undetectable. Counts of anti-inflammatory bacteria—microbes that specialize in fermenting nondigestible fibers—had increased. But could Zhao prove that these microbial changes caused anything? After all, the regimen may have simply contained far fewer calories than the patient’s previous diet.

So Zhao introduced the Enterobacter into mice. They developed endotoxemia, fattened up and became diabetic—but only when eating a high fat diet. Mice colonized with bifidobacteria and fed a high fat diet, meanwhile, remained lean, as did germ-free mice. The enterobacter was evidently unique, an opportunist. Aided by a high fat diet, the microbe appeared able to hijack the metabolism of both mice and man.

Zhao, who related his own story to Science last year, has repeated a version of this regimen in at least 90 subjects, achieved similar improvements, and has more than 1,000 patients in ongoing trials. He declined to be interviewed for this article, saying that the response to his research, both by press and individuals seeking advice, had been overwhelming. “I receive too many emails to ask for help but I can not provide much,” he wrote in an email. “I feel very bad about this and would like to concentrate on my research.”

There’s a flood of what you might call “fecoprospectors” seeking to catalog and preserve microbial diversity before it is lost in the extinction wave sweeping the globe.

Other researchers have tried an even more radical approach to treating the microbiome: the fecal transplant. It was originally developed to treat the potentially life-threatening gut infection caused by the bacterium Clostridium difficile. Studies so far suggest that it’s 95 percent effective in ousting C. diff. and has no major side effects. “Fecal engraftment” is now being considered a method for rebooting microbiota generally. Scientists at the Academic Medical Center in Amsterdam mixed stool from lean donors with saline solution and, via a tube that passed through the nose, down the throat and past the stomach, introduced the mixture to the small intestine of nine patients with metabolic syndrome. Control subjects received infusions of their own feces.

Those who received “lean” microbes saw improvements in insulin sensitivity, though they didn’t lose weight and saw the improvements disappear within a year. But Max Nieuwdorp, senior author on the study, aims to conduct the procedure repeatedly to see if the “lean” microbes will stick. And when he’s identified which are important, he hopes to create an anti-obesity “probiotic” to be taken orally.

Probiotics are just bacteria thought to be beneficial, like the lactobacilli and other bacteria in some yogurts. In the future probiotics might be bacteria derived from those found in Amazonian Indians, rural Africans, even the Amish—people, in other words, who retain a microbial diversity that the rest of us may have lost. Already, the literature suggests that a gold rush has begun—a flood of what you might call “fecoprospectors” seeking to catalog and preserve the diversity and richness of the ancestral microbiota before it is lost in the extinction wave sweeping the globe.

Ultimately, the strongest evidence to support microbial involvement in obesity may come from a procedure that, on the face of it, has nothing to do with microbes: gastric bypass surgery. The surgery, which involves creating a detour around the stomach, is the most effective intervention for morbid obesity—far more effective than dieting.

Originally, scientists thought it worked by limiting food consumption. But it’s increasingly obvious that’s not how the procedure works. The surgery somehow changes expression of thousands of genes in organs throughout the body, resetting the entire metabolism. In March, Lee Kaplan, director of the Massachusetts General Hospital Weight Center in Boston, published a study in Science Translational Medicine showing a substantial microbial contribution to that resetting.

He began with three sets obese mice, all on a high-fat diet. The first set received a sham operation—an incision in the intestine that didn’t really change much, but was meant to control for the possibility that trauma alone could cause weight loss. These mice then resumed their high fat diet. A second set also received a sham operation, but was put on a calorically restricted diet. The third group received gastric bypass surgery, but was then allowed to eat as it pleased.

As expected, both the bypass mice and dieted mice lost weight. But only the bypass mice showed normalization of insulin and glucose levels. Without that normalization, says Kaplan, mice and people alike inevitably regain lost weight.

“I won’t argue that all the effects of the gastric bypass can be transferred by the microbiota. What we’ve found is the first evidence that any can.”

To test the microbial contribution to these outcomes, Kaplan transplanted the microbiota from each set to germ-free mice. Only rodents colonized with microbes from the bypass mice lost weight, while actually eating more than mice colonized with microbes from the other groups.

In humans, some studies show a rebound of anti-inflammatory bacteria after gastric-bypass surgery. Dandona has also noted a decline in circulating endotoxin after the procedure. “I would never argue, and won’t argue, that all the effects of the gastric bypass can be transferred by the microbiota,” says Kaplan. “What we’ve found is the first evidence that any can. And these ‘any’ are pretty impressive.” If we understand the mechanism by which the microbiota shifts, he says, perhaps we can induce the changes without surgery.
NOW, NOT EVERYONE ACCEPTS that inflammation drives metabolic syndrome and obesity. And even among the idea’s proponents, no one claims that all inflammation emanates from the microbiota. Moreover, if you accept that inflammation contributes to obesity, then you’re obligated to consider all the many ways to become inflamed. The odd thing is, many of them are already implicated in obesity.

Particulate pollution from tailpipes and factories, linked to asthma, heart disease, and obesity, is known to be a cause of inflammation. So is chronic stress. And risk factors may interact with each other: In macaque troops, the high-ranking females, which experience less stress, can eat more junk food without developing metabolic syndrome than the more stressed, lower-ranking females. Epidemiologists have made similar observations in humans. Poorer people suffer the consequences of lousy dietary habits more than do those who are wealthier. The scientists who study this phenomenon call it “status syndrome.”

Exercise, meanwhile, is anti-inflammatory, which may explain why a brisk walk can immediately improve insulin sensitivity. Exercise may also fortify healthy brown fat, which burns off calories rather than storing them, like white fat does. This relationship may explain how physical activity really helps us lose weight. Yes, exercise burns calories, but the amount is often trivial. Just compensating for that bagel you ate for breakfast—roughly 290 calories—requires a 20-minute jog. And that’s not counting any cream cheese. Sleep deprivation may have the opposite effect, favoring white fat over brown, and altering the metabolism.

Brain inflammation precedes weight gain, suggesting that the injury might cause, or at least contribute to, obesity.

Then there’s the brain. Michael Schwartzdirector of the Diabetes and Obesity Center of Excellence at the University of Washington in Seattle, has found that the appetite regulation center of the brain—the hypothalamus—is often inflamed and damaged in obese people. He can reproduce this damage by feeding mice a high-fat diet; chronic consumption of junk food, it seems, injures this region of the brain. Crucially, the brain inflammation precedes weight gain, suggesting that the injury might cause, or at least contribute to, obesity. In other words, by melting down our appetite control centers, junk food may accelerate its own consumption, sending us into a kind of vicious cycle where we consume more of the poison wreaking havoc on our physiology.

Of course there’s a genetic contribution to obesity. But even here, inflammation rears its head. Some studies suggest that gene variants that increase aspects of immune firepower are over-represented among obese individuals. In past environments, these genes probably helped us fight off infections. In the context of today’s diet, however, they may increase the risk of metabolic syndrome.

Whether inflammation drives obesity or just contributes, how much of it emanates from our microbiota, or even whether it causes weight gain, or results from it—these are still somewhat open questions. But it is clear that chronic, low-grade inflammation, wherever it comes from, is unhealthy. And as Dandona discovered all those years ago, food can be either pro- or anti-inflammatory. Which brings us back to the question: What should we eat?
FIFTY YEARS AGO, due to the perceived link with heart disease, nutritionists cautioned against consuming animal fats and recommended hydrogenated vegetable oils, such as margarine, instead. Alas, it turned out that these fats may encourage the formation of arterial plaques, while some fats that were discarded—in fish and olive oil, for example—seem to prevent cardiovascular disease and obesity.

As people unwittingly cut out healthy fats, they compensated by consuming more sugar and other refined carbohydrates. But a high-sugar diet can produce endotoxemia, fatty liver, and metabolic syndrome in animals. So that’s yet another reason to avoid refined, sugary foods.

What about popular weight loss regimes, like the Atkins diet, that emphasize protein? In a 2011 study by scientists at the University of Aberdeen, in Scotland, 17 obese men were given a high-protein, low-carb diet. It prompted a decline of anti-inflammatory microbes, whose fermentation byproducts are critical to colonic health, and produced a microbial profile associated with colon cancer. So although it may prompt rapid weight loss, a high-protein, low-carb diet may predispose people to colon cancer. In the rodent version of this experiment, the addition of a prebiotic starch blunted the carcinogenic effect. Again, it’s not only what’s present in your diet that matters, but also what’s absent.

So, should we sprinkle a packet of fiber on our cheeseburger? Dandona has looked at this possibility and says that though this study has not yet been published, he’s found that packeted fiber does, when eaten with a fast-food meal, soften the food’s inflammatory effects. Fast-food companies could, in theory, pack their buns full of prebiotics, shielding their customers somewhat from metabolic syndrome.

But that’s not really what Dandona or anyone else is advocating. The pill approach—the idea that we can capture a cure in a gel cap—may be part of what got us in trouble to begin with. Natural variety and complexity have their own value, both for our own bodies and for our microbes. This may explain why orange juice, which contains plenty of sugur, doesn’t have inflammatory effects while a calorically equivalent quantity of sugar water does. Flavonoids, other phytochemicals, vitamins, the small amount of fiber it carries, and other things we have yet to quantify may all be protective.

Fast-food companies could, in theory, pack their buns full of prebiotics, shielding their customers somewhat from metabolic syndrome.

To that end, consider a study by Jens Walter (PDF), a scientist at the University of Nebraska-Lincoln. He supplemented the diet of 28 volunteers with either brown rice, barley, or both. Otherwise, they continued eating their usual fare. After four weeks, those who consumed both grains saw increased counts of anti-inflammatory bacteria, improved insulin sensitivity, and reduced inflammation—more so than subjects who just had one grain. Walter doesn’t think it’s an accident that those who ate both barley and brown rice saw the greatest improvement. The combination likely presented microbes with the largest array of fermentable fibers.

Scientists are also intensely interested in concocting “synbiotics,” a mixture of probiotic bacteria and the prebiotic fibers that feed them. This type of combination may already exist in staple dishes and garnishes, from sauerkraut to kefir, in traditional cuisines the world over.  In theory, such unpasteurized, fermented foods that retain their microbial communities are a health-producing triple whammy, containing prebiotic fibers, probiotic bacteria, and healthful fermentation byproducts like vitimins B and K. A smattering of recent studies suggest that embracing such grub could protect against metabolic syndrome. In one monthlong trial on 22 overweight South Koreans, unpasteurized fermented kimchi, which is made from cabbage, improved markers of inflammation and caused very minor decreases in body fat. Fresh, unfermented kimchi also helped, but not as much. In another double-blind, placebo-controlled study on 30 South Koreans, a pill of fermented soybean paste eaten daily for 12 weeks decreased that deadly visceral fat by 5 percent. Triglycerides, a risk factor for heart attacks, also declined. An epidemiological study, meanwhile, found that consumption of rice and kimchi cut the odds of metabolic syndrome. It all hints at a future where sauerkraut, kimchi, sour pickles, and other fermented foods that contain live microbial cultures do double duty as anti-obesity medicine.

So what else to eat? Onions and garlic are especially rich in the prebiotic fiber inulin, which selectively feeds good bacteria within. Potatoes, bananas, and yams carry loads of digestion-resistant starches. Apples and oranges carry a healthy serving of polysaccharides (another form of prebiotic). Nuts and whole grains do as well. Don’t forget your cruciferous vegetables (cabbage, broccoli, and cauliflower) and legumes. There’s no magic vegetable. Yes, some plant products are extra rich in prebiotics—the Jerusalem artichoke, for example—but really, these fibers abound in plants generally, and for a simple reason: Plants store energy in them. That’s why they’re resistant to degradation. They’re designed to last. (For more on what foods to eat, see “Should I Take A Probiotic?“)

The very qualities that improve palatability and lengthen shelf life—high sugar content, fats that resist turning rancid, and a lack of organic complexity—make refined foods toxic to your key microbes. Biologically simple, processed foods may cultivate a toxic microbial community, not unlike the algal blooms that result in oceanic “dead zones.”

In fact, scientists really do observe a dead zone of sorts when they peer into the obese microbiota. Microbes naturally form communities. In obese people, not only are anti-inflammatory microbes relatively scarce, diversity in general is depleted, and community structure degraded. Microbes that, in ecological parlance, we might call weedy species—the rats and cockroaches of your inner world—scurry around unimpeded. What’s the lesson? Junk food may produce a kind of microbial anarchy. Opportunists flourish as the greater structure collapses. Cooperative members get pushed aside. And you, who both contain and depend on the entire ecosystem, pay the price.

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Can Endurance Sports Really Cause Harm? The Lipopolysaccharides of Endotoxemia and Their Effect on the Heart

Also See:
Endotoxin: Poisoning from the Inside Out
Ray Peat, PhD on Endotoxin
Exercise Induced Stress
Stress — A Shifting of Resources
Exercise and Endotoxemia
Carbohydrate Lowers Exercise Induced Stress
Low carb + intensive training = fall in testosterone levels
Exercise and Effect on Thyroid Hormone
Exercise Induced Menstrual Disorders
Ray Peat, PhD: Quotes Relating to Exercise
Ray Peat, PhD and Concentric Exercise
Potential Adverse Cardiovascular Effects from Excessive Endurance Exercise
Running on Empty
How does estrogen enhance endotoxin toxicity? Let me count the ways.
Bowel Toxins Accelerate Aging
Ray Peat, PhD on the Benefits of the Raw Carrot
Protection from Endotoxin
Endotoxin-lipoprotein Hypothesis
Protective Bamboo Shoots
The effect of raw carrot on serum lipids and colon function
Are Happy Gut Bacteria Key to Weight Loss?

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(I personally don’t agree with the treatment options listed, but the actions of LPS during stress and exercise are valid and worthy of your time especially considering the exercise world’s complete ignorance of the topic. -FPS)

by Gary Huber, DO, AOBEM
Source

The endurance athlete is viewed as a model of aerobic efficiency, possessing tremendous cardiovascular health. Certainly we can agree that exercise induces a great number of benefits to our physiology and greatly improves the quality of life, but evidence exists that excessive exercise can cause cardiovascular damage. The heavy endurance athletes such as triathletes, marathon runners, and cyclists spend hours upon hours in a state of physiologic stress. Was the human body truly built to withstand this repetitive high oxidative stress exposure? There is literature to suggest that for some, the damage caused by ischemia to the bowel and the resultant endotoxemia leads to vascular and myocardial damage that in fact increases the risk for arrhythmic and atherosclerotic change. This article is written by an endurance sport enthusiast, so it is not intended to derail such activities but rather to explore this issue of lipopolysaccharides (LPS) and the cardiac damage that occurs so that we can ascertain the true risk involved and explore options for avoidance.

In a US population of more than 300 million people, 350,000 sudden cardiac deaths, or 111 events per 100,000 people, occur annually. Within this population, we understand that risk is secondary to lifestyle, age, and a host of other factors such as the building inflammation that often accompanies poor lifestyle and dietary decisions. But in a youthful age group who is exercising, we don’t expect sudden cardiac deaths. We have all heard tragic stories of the young athlete who dies on the field only to discover that he had an undiagnosed valvular or vascular defect. But there are a significant number of cases in which no identifiable anatomical defect can be found, yet the cause of death is listed as cardiac in nature. In a well-known study by Harmon published in 2011 in the journal Circulation, they reported a sudden cardiac death rate of NCAA athletes of 1 per 44,000 annually, or roughly 2.3/100,000.1 This might seem high, given that we are speaking of young athletes; but a look at CDC population-based data shows that cardiac-related death in the general population aged 15 to 24 is 2.5 per 100,000 people.2-5

One of the problems with the Harmon study is that the researchers did not document autopsy findings, and we are left to guess at the actual cause of cardiac death. This problem appears to be related to increased intensity of training, as the death rate is increased 2-fold from high school athletes to those on college teams.6,7

A 25-year review of autopsies in military recruits by Eckart showed a higher than expected rate of nontraumatic death at 13 per 100,000 recruits per year.8 86% of these deaths were related to exercise. Of those determined to be cardiac in origin, 61% were secondary to coronary artery pathology. The surprising finding is that despite autopsy, 35% of deaths determined to be nontraumatic sudden death were idiopathic. Another 20% of the cardiac deaths were diagnosed as myocarditis. Is it possible that the physical demand of these recruits played a role in the idiopathic and myocarditis deaths? That is an issue worth exploring through the lens of endotoxemia.

It has been demonstrated that LPS from gram-negative bacteria adversely affects cardiomyocytes, leading to apoptotic cell death.9-12 It is this apoptotic cell death that directly contributes to other forms of heart failures such as myocarditis, congestive heart disease, diabetic cardiomyopathy, chronic pressure overload, and ischemia-reperfusion injury.13-21 So as we view the myocarditis, arrhythmic, and other cardiovascular deaths in athletes, we have to ask, is it possible that the very activities which we love – our endurance sports – are acting as the nidus for LPS toxicity that is poisoning our hearts?

Defining the Problem
Engaging in prolonged endurance training or endurance events creates multiple physiologic stressors to alter our physiology. Blood flow must be redirected from central gut and liver to the peripheral muscle mass as well as the skin to facilitate heat release. This leads to a relative bowel ischemia as the splanchnic blood flow is reduced by 80%.22-24 Further exacerbating this ischemia is the simple volume loss due to sweat, the mechanical damage from the microtrauma of running, as well as thermal insult from rising body temperatures that all combine to worsen the mucosal damage occurring in the gut lining.25,26 This shock-induced damage results in loss of intestinal wall integrity and death to gram-negative organisms. The cell walls of gram-negative bacteria are composed of LPS, also known as endotoxins. LPS comprise 75% of the cell walls of gram-negative bacteria, and a single gram-negative bacterial cell wall can release 1 million LPS molecules into circulation.27,28

Excessive release of LPS secondary to bowel ischemia and loss of barrier effect can overwhelm the portal circulation and the Kupffer cells’ ability to neutralize them, resulting in entry to the general circulation where they cause significant adverse symptoms. The intestinal permeability induced by these sporting activities is thought to explain the high rate of occurrence of GI complaints such as diarrhea, cramps, and vomiting.29-31 The occurrence of GI issues has been reported to range from 30% to 93% of all endurance athletes and represents a common problem that is often unrecognized as a serious sign of endotoxemia. Recall that LPS endotoxemia is the process of sepsis, so other sepsislike symptoms may emerge, including fever, shivering, headache, and muscle ache.32-38

Endurance training clearly taxes liver function, as demonstrated by the Moncada-Jimènez study wherein endurance athletes completing a duathlon demonstrated endotoxemia in 50% of participants.39 Beyond that, all participants showed an increase in both AST and ALT level after their event. This reflects that during periods of endurance training, the reduction in splanchnic blood flow leading to bacterial death and translocation across the intestinal wall enter the portal circulation to reach the liver and induce the acute phase response. This same finding has been demonstrated in all types of endurance sport athletes, including cyclists, marathoners, and others.40-42

Sepsis represents our best understanding of endotoxins. Patients with sepsis experience fever, dizziness, GI complaints, shivering, and cardiovascular collapse secondary to the LPS presence in the bloodstream. I would contend that if you have ever watched someone finish a marathon, the temperature regulation issues, the gut effects, the shivering, and other symptoms that occur are just a milder version of sepsis. The mechanism is the same, and unfortunately the cardiovascular risk is a part of this picture. Yes, endurance athletes are jeopardizing their heart health and potentially causing heart damage every time they train and compete. Their cardiovascular efficiency may be enhanced, but the LPS release is causing myocyte damage.

LPS can cause direct stimulation of cytokines, including TNF-alpha, which leads to severe problems; but low levels of LPS can cause damaging effects without the stimulation of cytokines. There is a multilevel response potential such that low levels of circulating LPS can cause cardiac apoptosis without stimulating excess cytokine response. It has a direct toxicity beyond its cytokine effect by directly engaging the myocyte via the toll-like receptor-4 (TLR-4).43 Low levels in the nanogram-per-milliliter range can alter myocyte function.44,45

LPS can stimulate cardiac myocytes to release TNF-alpha and nitric oxide to induce apoptosis via an autocrine manner, but this level of damage occurs in the microgram/ml range. LPS at low levels does not rely on NO or TNF-alpha to cause apoptosis.46-49

So LPS exposure, whether high dose in micrograms or low dose in nanograms, has multiple mechanisms of action to induce cardiac damage. LPS in low doses (10 ng/ml) decreased the ratio of the antiapoptotic protein Bcl-2 relative to the proapoptotic protein Bax, thus influencing apoptosis. The Li study showed that in vivo use of LPS in low dose caused a 2-fold increase in apoptosis that was blocked by the use of losartan.50 The ability of LPS to independently induce apoptosis outside cytokine contribution is via stimulation of cardiac AT1 receptors. Angiotensin II induces caspase-3 enzymes which trigger apoptosis.51,52 A single low dose of LPS that caused no appreciable distress and no adverse impact on blood pressure was sufficient to increase cardiac apoptosis. Low levels of LPS have been shown to be clinically relevant in multiple disease processes without causing overt distress or blood pressure changes.53-55

In the Jeukendrup study, 29 triathletes were followed with blood test before and after an Ironman distance triathlon, and a full 93% reported GI issues; 68% had endotoxemia defined as LPS levels >5 pg/ml.56 Other measures of note were IL-6 levels elevated 27-fold and CRP increased 20-fold. Interestingly, this study followed these athletes with blood measures 16 hours after the race and found that the rate of endotoxemia had increased from 68% to 79% at the 16-hour mark, demonstrating the extended effect of such physical efforts. The prealbumin level was reduced by 12%, consistent with acute phase reactions wherein the body directs efforts in making CRP and fibrinogen at the expense of making albumin and prealbumin. This is expected in the face of high CRP which was documented. In another extreme endurance event, Brocke-Utne demonstrated an endotoxemia occurrence rate of 81%.57

A Look at the Cellular Mechanism of Endotoxemia
LPS in the circulation binds LBP (lipopolysaccharide binding protein) to form a complex LPS-LBP which binds to the cell membrane of Kupffer cells, reacting with the TLR-4 receptor and triggering the activation and translocation of NF-kB.58,59 So both the endotoxin and the oxidative stress of intense sporting activity induce production of NF-kB, thus upregulating pro-inflammatory cytokines.

LPS release causes activation of the coagulation and the complement cascade.

The pathway for this activity is through the toll-like receptor 4 (TLR-4). Cardiac myocytes express TLR-4 receptors and are susceptible to direct damage by LPS exposure.44,45,60,61

LPS stimulation of TLR-4 receptors causes depression of the myocyte contractility; they impair beta-adrenergic reactivity, and induce apoptosis through the cardiac renin-angiotensin system and the angiotensin type 1 receptors. This stimulation can lead to cardiac fibrosis.9-12, 62-66

In studies by Lew et al. in 2013, researchers exposed mice to low levels of LPS that caused no discernible clinical adverse events and yet with chronic exposure demonstrated development of fibrosis and increased mortality.66 Lew et al. found that the use of losartan, which had previously been shown effective in Li’s study, had no effect in their mouse model.

Mechanisms for LPS exposure include67-70:
1. sports, endurance activity, strenuous exercise
2. high-fat meals
3. periodontal disease
4. chronic type 2 diabetes
5. smoking
6. chronic infections, URIs, etc.
7. metabolic syndrome
8. cirrhosis
9. heart failure

These can cause levels of LPS in the picogram to nanogram/ml range.71

Chronic recurrent exposure of LPS by athletes can be compared to the low chronic levels of exposure seen with people with periodontal disease, smokers, chronic infections, or chronic heart failure.72 These low levels of LPS are seen in humans with chronic heart failure, suggesting a slow destructive apoptotic occurrence.

This is eerie with relation to the NCAA athletes or the military recruit studies. In Lew’s study, the mice received low doses of LPS on a weekly basis, showing mild transient effects that resolved within hours. Sounds like symptoms associated with doing a hard interval workout or a long training ride. The LPS-treated mice appeared normal, with good activity and normal hemodynamic measures, including normal LV size and function, but then over time demonstrated an increased mortality with unexpected deaths. This sounds like endurance training with weekly doses of hard efforts that release LPS, causing transient symptoms and low-IgG anti-LPS levels, while causing cardiac fibrosis and apoptosis, resulting in an increased risk for sudden cardiac death which has been documented.

Short-term benefits may be seen with our innate immune response to transient inflammation. Mann’s experiments, which employed a short-term preload with LPS, demonstrated a protective effect, similar to the concept of hormesis.73 But he went on to report that the chronic nature of the inflammatory process of repeated LPS exposure is damaging, leading to atherosclerosis. The recurrent activation of TLR-4 is damaging to cardiovascular health and produces fibrosis of the myocyte.

LPS is involved in plaque rupture and vascular signaling. TLR-4 is upregulated and concentrated in the shoulder region of plaque, which is where rupture most commonly occurs. There is a clear association between bacterial infection and, in the case of our endurance athletes, chronic bacterial LPS exposure and the development of atherosclerosis. TLR-4-induced inflammation has been linked to plaque instability, and potential for acute coronary syndrome.73

The review by Venardos discusses the importance of myocardial antioxidant enzyme systems such as the glutathione peroxidase (GPX) and the thioredoxin reductase (TxnRed) system and their important role against oxidative stress and recovery in cardiac tissue.20 The GPX and TxnRed are both selenocysteine-dependent enzymes. The sweat losses of all minerals, not the least of which are selenium, iodine, and magnesium, play a role in elevating risk; and their absence reduces myocytes’ ability to withstand oxidative challenges.

Defining Endotoxemia in Various Reports
Endotoxemia is defined as an LPS level greater than 5 pg/ml. In reviewing this literature, various definitions have been employed as well as various tests and reagents to identify it; and as such, several factors need to be taken into consideration. Depending on the reagent used and whether methods to remove LPS inhibitory substances are used, the level can vary widely. For example some reagents used to measure LPS are also sensitive to B-glucan from fungi, so use of this type of test will yield higher levels of LPS being reported. These are the factors that create confusion when comparing studies but the evidence is still greatly significant in well-controlled studies using proper reagents that LPS is real and problematic.

Chronic effect of LPS exposure
Anti-LPS antibodies are produced by the body to bind LPS when present. These levels are lower in endurance athletes both before and after endurance events and thought to represent the chronic low levels of LPS occurring in these athletes from regular training resulting in “drainage” of adequate levels of IgG anti-LPS.74,75

There is chronic leakage of LPS secondary to long-term mucosal damage and recurrent efforts leading to low IgG anti-LPS and thus the suspicion of chronic cardiac exposure to LPS and myocyte damage. The fact that TNF-alpha may not be detected in the blood is not a surprise, as TNF-alpha has a very short half-life, and even in patients with documented sepsis, the presence of TNF is typically only found in 4% to 54% of patients.76

We know that endurance athletes struggle with frequent upper respiratory tract infections (URI) secondary to the immune suppressive effect of their sport.77 Immune suppression after extreme efforts has been documented to last for 3 to 72 hours post exertion.78 The stress incurred by the HPA axis and all of the resultant immune and cytokine reactions result in a decline in the IgA levels, leaving the gut unprotected and vulnerable to barrier defects.78 The simple application of vitamin C has been shown to reduce URI frequency post endurance events.79

Treatment
As stated in the opening of this article, the goal is not to condemn endurance sports but rather understand the potential risk of damage of such activity and proceed in a manner that not only ensures greater health but likely improves athletic performance as well. There are several well-studied approaches that offer promise as well as safety in their application.

Resveratrol suppresses endotoxin-induced production of pro-inflammatory cytokines and activates the Nrf2 antioxidant defense pathway in vivo. Classic elevation in creatine kinase (CK) and lactate dehydrogenase (LDH) is seen with cardiac damage secondary to exposure to LPS. Hao, employing an in vivo mouse study, demonstrated that pretreatment with resveratrol significantly reduced LPS-induced elevation in CK and LDH.80 Echocardiogram demonstrated a preservation of ejection fraction that had previously been reduced in the face of LPS administration. These investigators further pursued this topic by culturing human cells in LPS with resveratrol and demonstrated a significant reduction in apoptosis and necrosis in the resveratrol cultured cells.

Vitamin C reduces bacterial overgrowth, and endotoxemia, and reduces the intestinal barrier defect. Vitamin C in doses of just 1000 mg prior to a significant training effort has been shown to be effective in producing a protective antioxidant effect, maintains the gut barrier effect, and reduces LPS leakage into the circulation.81

Patients with IBD, a common condition found in endurance athletes, show significantly reduced levels of vitamin C in mucosal tissue compared with non-IBD controls.82 The study by Abhilash showed that vitamin C improved the integrity of mucosal tissue, reduced damage from LPS, protecting the liver and reducing fibrosis secondary to oxidative insult.83

Lactobacillus plantarum produces lipoteichoic acid (LTA), which has been shown to reduce LPS-induced TNF-alpha expression and downregulate the TLR-4 activity.84,85 The goal with this type of treatment is to produce tolerance against the effects of LPS. Reducing the acute LPS effect may translate into reduction of the cumulative cardiovascular damage long term.

Curcumin has been employed for a multitude of benefits related to reduction in inflammation. Its use in the treatment of inflammatory bowel disease and inhibition of ulcer formation has been well studied and documented. Constituents of curcumin have a protective effect and inhibit intestinal spasm while increasing gastrin, secretin, bicarbonate, pancreatic enzyme, and mucous secretion.86

Turmeric’s anti-inflammatory activity may lead to improvement in obesity and obesity-related diseases such as heart disease and diabetes. Curcumin interacts with hepatic stellate cells and macrophages, wherein it suppresses several cellular proteins such as transcription factor NF-kB and STAT-3, and activates Nrf2 cell signaling pathway.87

In a 2009 study, curcumin was used to block the muscle-wasting effects of LPS.88 There was a dose dependent reduction in muscle loss in mice injected with LPS. Curcumin inhibited p38 kinase activity (involved in stress-induced apoptosis) in LPS-affected muscle.89 Knowing the muscle-wasting effects of endurance sports in conjunction with the known release of LPS, curcumin would seem a safe and natural approach for reduction of oxidative stress and preservation of bowel function and integrity.

One last variable needs consideration in this topic. Chagnon cited evidence in 2005 of a cardiac-derived myocardial depressant factor known as macrophage migration inhibitory factor (MIF).12 It appears that MIF is a critical piece to the mechanism of cardiac damage from LPS, yet its exact mechanism remains unclear. MIF is released from myocardium in response to LPS and acts as an inflammatory mediator, disrupting immune homeostasis. In a mouse study wherein investigators employed an anti-MIF antibody they were able to demonstrate a complete blockade of the LPS effect on myocytes. The blockade of MIF resulted in an increase in Bcl2/Bax ratio (an antiapoptotic result), inhibiting the release of mitochondrial cytochrome c, which in turn prevents caspase 3 activation (another antiapoptotic effect) and reduces DNA fragmentation.

Given that MIF is in fact an inflammatory mediator in immune homeostasis, it is quite possible that the multidimensional impact of resveratrol, vitamin C, and curcumin is having a direct effect on MIF. Given that these botanicals and nutrients have multiple mechanisms of action, including effects on mitochondrial function, PGC-1a, cyclooxygenase enzymes, NF-kB, and cytokine production, including TNF-alpha, their combined impact may indeed block cardiovascular damage.

A controlled study to assess the combined impact of these protective elements on endurance athletes will likely never be done; but given the information discussed here, I think that it is more than prudent to share this approach with all endurance athletes, as it represents the potential for reducing sudden cardiac events and promoting greater health overall.

Correspondence:
8170 Corporate Park Dr.
Cincinnati Ohio 45242
ghuber@huberpm.com

Notes
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Dr. Gary Huber is president of the LaValle metabolic institute. He spent 20 years as an emergency medicine physician before joining Jim LaValle in the practice of integrative medicine at LMI. Dr. Huber is an adjunct professor teaching integrative medicine practice at the University of Cincinnati College of Pharmacy as well as a clinical preceptor for pharmacy students. Dr. Huber also lectures on hormone replacement therapies and integrative care for the American Academy of Anti-Aging Medicine for the University of South Florida. He has developed the Metabolic Code Professional Weight Loss Program that has proved very beneficial in reversing metabolic syndrome issues. Dr. Huber has a long-held interest in nutrition and human physiology as it relates to wellness and longevity. He has served as medical director for the Flying Pig Marathon and is presently on the board of directors for Loveland’s Amazing Race, a local charity event.

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