Here is a post on the CR Message Boards from Paul McGlothin about how stress can shorten telomeres! Here is the post! Read up! THANK YOU Paul for making us aware of these papers!

For those of you who want to cut straight to the research papers, here are their PubMed Links:

Accelerated telomere shortening
in response to life stress.

December, 2004 [FREE Article!!!] PMID: 15574496

Here we provide evidence that psychological stress–both perceived stress and chronicity of stress–is significantly associated with higher oxidative stress, lower telomerase activity, and shorter telomere length, which are known determinants of cell senescence and longevity, in peripheral blood mononuclear cells from healthy premenopausal women. Women with the highest levels of perceived stress have telomeres shorter on average by the equivalent of at least one decade of additional aging compared to low stress women.

Cell aging in relation to stress arousal and cardiovascular disease risk factors.

April 2006 [Abstract Only for Free] PMID:16298085

Here we examine whether telomere length and telomerase in leukocytes are associated with physiological signs of stress arousal and CVD risk factors in 62 healthy women. Low telomerase activity in leukocytes was associated with exaggerated autonomic reactivity to acute mental stress and elevated nocturnal epinephrine. Further, low telomerase activity was associated with the major risk factors for CVD -smoking, poor lipid profile, high systolic blood pressure, high fasting glucose, greater abdominal adiposity-as well as to a composite Metabolic Syndrome variable. Telomere length was related only to elevated stress hormones (catecholamines and cortisol). Thus, we propose that low leukocyte telomerase constitutes an early marker of CVD risk, possibly preceding shortened telomeres, that results in part from chronic stress arousal.

Dynamics of telomerase activity
in response to acute psychological stress.

May 2010 [Abstract Only for Free] PMID:20018236

Telomerase activity plays an essential role in cell survival, by lengthening telomeres and promoting cell growth and longevity. It is now possible to quantify the low levels of telomerase activity in human leukocytes. Low basal telomerase activity has been related to chronic stress in people and to chronic glucocorticoid exposure in vitro. Here we test whether leukocyte telomerase activity changes under acute psychological stress…..These findings uncover novel relationships of dynamic telomerase activity with exposure to an acute stressor, and with two classic aspects of the stress response – perceived psychological stress and neuroendocrine (cortisol) responses to the stressor.

So Stressed…..

Also, I just started reading a book that y’all may be interested in. My Mother bought this for me, and I think she picked out a pretty good book! It’s called

“So Stressed:
The Ultimate Stress Relief Plan for Women”

by Stephanie McClellan M.D. and Beth Hamilton M.D.

I have only started it, but when I finish it I will put up a review in my book section!

I’m on a curry kick right now, but I wanted to try something other than my red curry. I have a big jar of yellow curry in the fridge that I decided to put to good use, and it’s vegan. If you are wanting to keep it vegan, make sure you check curry paste ingredients because some will put fish sauce or shrimp paste in them.

Thai Yellow Curry & Vegetables

(~12 servings)

2C Water
4 Cans Lite Coconut Milk
1T Vegetable Bullion
240g Onion, diced fine
320g Eggplant, diced fine
250g Broccoli, coarsely chopped
500g Carrots, sliced
100g Sweet Pepper, sliced or chopped
440g Snow peas, chopped in half or thirds
2x15oz cans Black Beans, drained and rinsed
2x 8oz Shiratake Noodles, chopped
90g Lundberg Wild Rice
150g Yellow Curry Paste
10g Nutritional Yeast
30g Thai Basil (jar, but fresh if you can get it)
30g Lemon Grass (in a jar, but I’m sure fresh would work too)

Optimal: Thai Chilies…I like to add Super Hot Crushed to my bowl. YUM.

Put the 2C of water in a large pot on med heat. Dissolve the bullion, then add the chopped onion, pepper, and eggplant. Dissolve the curry paste in some of the coconut milk, making sure there are no lumps, then add to the pot. Add the basil and lemon grass. Go ahead and add all the coconut milk to the pot. Add the rice, and as you chop the rest of the veggies add them. Just make sure the rice simmers in the pot for about 45min. I like to add the snow peas about 5 min before I take up the pot, so they are still slightly crunchy…but it’s your choice.

===========================================
Nutrition Summary for November 9, 2010
Report generated by CRON-o-Meter v0.9.7
===========================================

General (18%)
===========================================
Energy               |   249.9 kcal    19%
Protein              |     9.3 g       16%
Carbs                |    35.0 g       18%
Fiber              |     9.4 g       38%
Starch             |     0.6 g        4%
Sugars             |     5.4 g       11%
Fat                  |     8.2 g       17%

Vitamins (51%)
===========================================
Vitamin A            |  7440.2 IU     149%
Lutein+Zeaxanthin  |   662.8 µg      13%
Folate               |   198.6 µg     110%
B1 (Thiamine)        |     1.0 mg      90%
B2 (Riboflavin)      |     0.9 mg      68%
B3 (Niacin)          |     6.0 mg      40%
B5 (Pantothenic Acid)|     0.9 mg      17%
B6 (Pyridoxine)      |     1.0 mg      62%
B12 (Cyanocobalamin) |     0.6 µg      29%
Vitamin C            |    53.1 mg      88%
Vitamin D            |     0.0 IU       0%
Vitamin E            |     0.8 mg       7%
Vitamin K            |    41.3 µg      46%

Minerals (24%)
===========================================
Calcium              |   100.4 mg      10%
Copper               |     0.2 mg      12%
Iron                 |     2.5 mg      17%
Magnesium            |    72.0 mg      22%
Manganese            |     0.6 mg      16%
Phosphorus           |   169.8 mg      24%
Potassium            |   595.8 mg      17%
Selenium             |     3.4 µg       6%
Sodium               |   660.2 mg     132%
Zinc                 |     1.6 mg      13%

Amino Acids (38%)
===========================================
CYS                  |     0.1 g       50%
ILE                  |     0.4 g       33%
LEU                  |     0.6 g       28%
LYS                  |     0.5 g       32%
MET                  |     0.1 g       22%
PHE                  |     0.4 g       43%
THR                  |     0.4 g       45%
TRP                  |     0.1 g       42%
TYR                  |     0.3 g       55%
VAL                  |     0.5 g       29%

Lipids (7%)
===========================================
Saturated            |     6.5 g       32%
Monounsaturated      |     0.1 g        0%
Polyunsaturated      |     0.3 g        1%
Omega-3            |     0.1 g        8%
Omega-6            |     0.2 g        2%
Cholesterol          |     0.0 mg       0%

Nutrition and aging skin: sugar and glycation.

Abstract:

The effect of sugars on aging skin is governed by the simple act of covalently cross-linking two collagen fibers, which renders both of them incapable of easy repair. Glucose and fructose link the amino acids present in the collagen and elastin that support the dermis, producing advanced glycation end products or “AGEs.” This process is accelerated in all body tissues when sugar is elevated and is further stimulated by ultraviolet light in the skin. The effect on vascular, renal, retinal, coronary, and cutaneous tissues is being defined, as are methods of reducing the glycation load through careful diet and use of supplements.

My concern for AGEs was one of the initial reason driving me toward a vegan diet. The second factor leading me to veganism was lowering protein; specifically leucine and methionine. Eating vegan diminishes these two dietary concerns. Eating low sugar vegan with a lot of raw or minimally cooked vegan foods is what I consider to be ideal for me right now. After making the transition to vegan for purely dietary reasons, I become re-familiarized with the reasons I became vegan the first time back in college after reading the book “Eating Animals“.

So, where am I going with this post? I wanted to provide you with a refresher or introduction to AGEs, and then I wanted to include a few more research papers I found relating to this topic. Since AGEs are a real concern, I feel it’s good to revisit this topic for renewed motivation to seek alternative foods and to practice informed supplementation.

So, what have I found?

The low-AGE content of low-fat vegan diets could benefit diabetics – though concurrent taurine supplementation may be needed to minimize endogenous AGE production.

I only have access to this abstract, but nonetheless this is still worth mentioning. This paper investigates the fact that while vegan diets, particularly low-fat vegan diets, are low in exogenous AGEs, some tests have revealed that vegans show a higher serum AGE content than omnivores. This suggests that something about the vegan diet can lead to a higher endogenous AGE production. One theory is a higher fructose consumption, but data has yet to support this. Another theory is that the lack of taurine in vegan diets may be partly responsible for AGE buildup. In the abstract, the researchers conclude that a low-fat vegan diet supplemented with taurine may be able to suppress elevated AGE production.

** I would really like to read the entire paper so I can further understand their diet analysis. Also, they focus on a low-fat vegan diet because such items as roasted nuts and broiled tofu are foods high in AGEs. Instead of going into good-bad fats and ways to prepare low-AGE fatty foods, they choose to cut fat content instead.

*** I supplement with taurine, and while I do eat a high fat diet I make sure I eat raw fats. My fat staples include avocado, flax oil, soon to be high quality olive oil, and coconut oil. Now, I will cook some with coconut oil, but because coconut oil is almost all saturated fat, it isn’t subject to the same lipoxidation as polyunsaturated fats. I also take carnosine to help with endogenous AGEs. IMO, a properly supplemented vegan diet that takes into concern type and preparation method of fats will be superior to an omnivore diet from an AGE perspective.

Would carnosine or a carnivorous diet help suppress aging and associated pathologies?

This is another stud which looks at the benefits of carnosine. Obviously, I don’t agree with the carnivorous diet, but I do agree with carnosine supplementation. Carnosine is known for it’s anti-glycation properties as well as it’s chelating ability with zinc and copper, reactivity with potentially destructive carbonyl groups, and possible activity against age-related protein carbonyl stress. Carnosine is also thought to help with neuro-degeneration.

This was an AGE refresher, and reminder to watch you AGEs!

My attention has recently been focused toward olive oil benefits as I accepted an invitation to buy some high-polyphenol olive oil from Spain. The initial proposal and discussion of olive oil concerns and potential benefits were convincing enough to buy now and learn later. Ha. So, here I am learning later. I’m sure most of us have at least heard olive oil has health benefits, but I’ve never really dissected the information. There are two in depth reviews on olive oil that I want to share. In a follow up post, I am going to discuss the quality problems with buying olive oil from your grocery store.

Biological Activities of Phenolic Compounds Present in Virgin Olive Oil

This is a very current review summarizing the current knowledge of the phenolic compounds in olive oil. Both in vitro and in vivo studies in animals and humans have shown the phenolic compounds in olive oil have beneficial effects on plasma lipoproteins, oxidative damage, inflammatory markers, platelet and cellular function, antimicrobial activity, and bone health.

Lower rates of heart disease and certain cancers in the Mediterranean region have been partially attributed virgin olive intake which ranges from 25-50ml/day.  Studies have correlated the health benefits of virgin olive oil to the highly bioavailable phenolic compounds, and at least 36 different phenolic compounds are known.

Variation in the concentration of phenolic compounds in olive oil is due to the region, agricultural techniques, maturation of fruit at harvest, oil extraction process, process, storage, and time since harvest. Also, cooking alters the concentration of phenolic compounds.

This review continues with a summary of the bioavailability of several phenolic compounds and their benefits. So, if you are interested in the specifics of the compounds, follow the title’s link for the pdf. Below is a neat diagram of the biological activities of the phenolic compounds in olive oil.

Top 3 Phenolic Compounds in Olive Oil:

Hydroxytyrosol
Tyrosol
Oleuropein

This review goes into detail the benefits of the phenolic compounds in olive oil, and the evidence seems pretty concrete. Trying to select healthy fats/oils as been a moderate concern of mine, and I think that buying some high quality olive oil to incorporate into my diet is a great start to picking the right fats.

So, between my food fats from raw nuts/seeds and avocados and then my oil fats from flax oil and now soon to be high-polyphenol olive oil, I think I have a great selection of fats/oils to pull from for a healthy diet. Since I do eat a higher fat diet, I want to consume the best fats I can. Fats seem to be an area of potential health danger if the wrong or over processed ones are selected, so my paranoia in this area seems legitimate based on what I have read.

**********************

Olive oil and health: Summary of the II international conference on olive oil and health consensus report

This is another similar interesting review on olive oil’s health benefits that is worth at least a quick glance.

Animal Protein Intake and Risk of Inflammatory Bowel Disease: The E3N Prospective Study.

Researchers wanted to study the proposed connection between animal protein consumption and increased risk for IBD.  The study consisted of 67,581 women living in France between the ages of 40-65 without major diseases at the beginning of the study. The study was conducted over 10.4 years, and questionnaires on lifestyle were given ever 24 months along with an clinical IBD assessment. During the study, a total of 77 cases of IBD were diagnosed during the study, and 458 women checked Crohn’s disease or Ulcerative Colitis on the questionnaire. (further details in link)

High protein intake, specifically animal protein, was significantly associated with increased risk of IBD (particularity for Ulcerative Colitis). Meat and fish, were particularly associated but not eggs or dairy (but eggs or dairy may not have been eaten in as large of quantities).

Specifics of the Results:

In the adjusted model, only total protein intake (not carbs or fats) was associated with an increased IBD risk. Interestingly, only animal protein exerted this IBD risk with no association observed with plant protein. Also, differences between UC (ulcerative colitis) and CD (Crohn’s Disease) were observed. CD was most correlated to total protein intake as opposed to animal or plant, while a strong association was seen with animal protein and UC.

How is moderate to high protein intake defined in this study?

Protein intake fell into three average intake groups. The first was 1.08g/kg, the second was 1.52g/kg, and the third intake group averaged in at 2.07g/kg. High protein intake saw a 3.3 fold risk of developing IBD.

Why might animal protein cause an increased IBD risk?

The small intestines do not adsorb some of the heme and amino acids contained in animal proteins. These are then passed to the colonic lumen and are metabolized by the micro-flora. Products from these reactions include hydrogen sulfide, phenolic compounds, amines and ammonia which are toxic to the colon.

Sulfide may alter the cell membrane of the intestinal wall cells leading to loss of barrier function which in turns triggers an immune response.

Even in healthy people, it has been shown that an increase in dietary protein leads to changes in colonic metabolism which is reflected by an increase in fecal ammonia, fecal volatile sulfur compounds, and urinary p-cresol.

Obviously, one limitation of this study was that it only included middle aged women, but these results highlight the need for additional studies in the younger and male population.

I wanted to cover this review to increase awareness of aging interventions and CR variations. Currently, Calorie Restriction is the most effective form of dietary intervention against aging. As confirming data continue to emerge, CR is gaining respect as not only a potential human life extension method, but a very viable method to increase health span. At the very least, Calorie Restriction can improve the quality of life and healthy years even if the longevity benefits are meager.

CR mimetic research continues try to find an agent able to reproduce the in vivo effects of CR without reducing calories. Understanding the mechanisms of CR would help lead to a CR mimetic. Non-CR dietary interventions against aging are known, but so far none are as effective. Below are the summaries of aging intervention agents and variations on CR.

Dietary Interventions to Extend Life Span and Health Span Based on Calorie Restriction

Antioxidants:

The free-radical theory of aging theorizes that reactive oxygen species (ROS) damage molecules and cell structures which in turn causes aging. Antioxidants are proposed to “neutralize” the oxidation species thus preventing damage. Despite the popularity of this theory, studies have not provided evidence that food based antioxidants prolong life or prevent aging, and some studies have even shown toxic effect of antioxidant supplementation. Given this information, antioxidant supplementation in humans is no longer recommended.

Glucose and Insulin Homeostasis:

Increased glucose intolerance and insulin resistance are often seen with aging. Because Calorie Restriction is known to improve or even reverse hyperglycemia and insulin resistance, CR mimetics targets for these results are being studied.

2-Deoxy-D-glucose (2DG):

2DG is a glucose analogue that inhibits glycolysis, and is being investigated as a CR mimetic due to its effects on energy metabolism. Preliminary findings have shown it’s ability to inhibit tumor growth, and increase stress resistance to neurotoxins and shock; however, recent finding have shown negative long term consequences and thus may only be useful in short term applications.

Biguanides:

The biguanide derivatives buformin, metformin, and phenformin are known to improve glucose homeostasis, and were effective treatment against diabetes mellitus and additionally showed promising tumor inhibition. Due to unfavorable side effects, metformin is the only compound still in use and is commonly used as treatment for type 2 diabetes. Metformin improves insulin sensitivity, and is known to reduce adiposity and mortality rates in diabetic people. However, it’s ability to actually extend life span in *healthy* rodents, primates, and humans is still unknown.

Advanced Glycation End Products:

AGEs are the product of excess glucose combining with proteins an can happen in vivo or during the cooking of food (although food items do have a smaller concentration of AGES even prior to cooking). These products then attract other proteins, forming web-like networks which in turn stiffen joints, block arteries, and could even cloud the eye lens thus leading to cataracts. Significant concentrations of AGEs are found in diabetic individuals as well as aging tissues. Componds that could prevent or reverse accumulation of such products may not only be an effect treatment for diabetes but also aging given the similarity of aging with diabetic complications. One study reported an increase in mean and max life span of rodents whose dietary intake of AGEs was reduced, and another reported that mice fed a high AGE CR diet did not receive the life extending benefits normally seen with CR.

Aminoguanidine:

Also known as pimagedine, aminoguanidine is no only the most studied AGE inhibitor, but also functions as a general antioxidant and inhibitor of diamine oxidase and nitric synthase. Even though this molecule was found to prevent arterial stiffening and cardiac hypertrophy in rats, it’s has not been proven to actually extend life span. Also in diabetic trials, despite it’s beneficial effects against retinopathy and serum lipids, negative side effects were reported.

Pyridoxamine (P5P):

Not only does this molecule inhibit AGEs, it also is known to prevent advanced lipoxidation reactions. This member of the vitamin B6 family has also been found to reduce the cross-linking associated with cataracts in mice, but further studies investigating the extent of its capabilities are required.

mTOR Signaling Pathway:

The mTOR pathway acts as a nutrient sensing pathway, and in mammals is now known to be a central regulator of energy homeostasis and cellular metabolism. The inhibition of this pathway in worms, flies, and yeasts is known to extend life span. Molecules that inhibit the mTOR pathway are becoming major candidates for CR mimetics as Calorie Restriction is known to inhibit mTOR signaling in multiple species.

mammalian target of rapamycin (mTOR)

Rapamycin:

This is a drug original used for it’s immunosuppressant actions, but it now known to selectively inhibit mTOR. Additional benefits include antibiotic, anti-tumor activity. Whether rapamycin could be used for long term human aging intervention is still unknown.

Sirtuin Activators:

On way Calorie Restriction is thought to extend life is though increasing the activity of sirtuins.  Specifically, the activation of human Sirt1 is thought to not only be able to increase life span, but also increase health span. Resveratrol was originally thought to be a Sirt1 activator, but recent studies have contradicted these findings.  Finding molecules that activate Sirt1 are of great interests for CR mimetics researchers.

Resveratrol:

Originally thought to be a legitimate CR mimetic after its ability to mimic CR in several short-lived species, this molecule that is found in red wine is now known not to carry it’s life extending properties to mice. However, it is able to mimic some health benefits of CR including glucose sensitivity, physical endurance, and gene transcription properties. In addition, resveratrol may be able to increase quality of life in overweight and elderly individuals.

Protein Restriction:

Several (but not all) studies have confirmed life extending benefits of low protein diets in rodents. Additional studies show evidence for the restriction of specific amino acids as a way to benefit health and longevity rather than protein restriction in general. Given that vegetarians have a reduced risk for for several chronic diseases of aging, more studies in this area are warranted.

Intermittent Fasting:

A similar but not equal dietary approach for human adaptation to a CR-like diet is intermittent fasting. By alternating ad lib and restricted eating periods, several benefits seen with CR may be attainable with this method. This is thought to be an alternative, easier long term solution for those who find practicing CR too difficult.

Conclusion:

Remember that CR is the only known way to extend life span and health span across species, but other methods mimicking some or -one day- all of the effects of CR may be able to pass on these benefits without restricting calories. Currently, there are many known ways to mimic some of the health span extending properties which still provide tangible benefits to humans. Both quality and quantity of life are important factors when considering both Calorie Restriction and CR mimetics.

In previous posts I’ve discussed, mTOR: the mammalian target of rapamycin. Studies in a variety of species support TOR as an aging regulator. During periods of dietary restriction, TOR signaling  affects processes involving mRNA translation, autophagy, stress signaling and response, and metabolism which in turn slows aging. A paper published in June 2010, provides more support for TOR as an aging modulator. I try to highlight some of the major/most interesting concepts, but this is a pretty detailed paper you may want to read for yourself.

With TOR, less is more: a key role for the conserved nutrient-sensing TOR pathway in aging.

(CR Society full copy)

Rapamycin is an immunosuppressive drug which inhibits TOR activity. TORC1 (TOR Complex 1), which plays a central role in TOR signaling network, is the specific TOR protein sensitive to rapamycin. TORC1 controls cell size, proliferation, and life span through several downstream pathways.

TOR Affects Growth Via Nutrient Sensing

TOR is sensitive to the reduction in nutrients across a wide array of species. During nutrient deprivation, TOR slows growth. In species modified to have reduced or no TOR signaling, development and growth is either comparable to that seen with nutrient deprived circumstances, or in some situations lacking TOR the lack of development is fatal.

TOR: Growth Factors and Stress

TORC1 can also be thought of as a signaling hub: receiving signals from a number a factors and in turn influencing multiple physiological responses. Because of this, TOR is thought of as a “growth checkpoint” -checking for favorable conditions and mediating growth in turn. Many of the cellular processes affects by TOR mediation are believed to influence life span.

TOR is not only sensitive to quantity of available nutrients, but the quality too. One powerful TOR inhibitor is the withdrawal of amino acids (the building blocks of protein). L-lucine is a major TOR activator, but L-tryptophan, L-phenylalanine, and L-arginine can also activator TORC1 when transported into a cell. TOR is also affect by cellular glucose levels. During a reduction in cellular energy, TOR signaling is reduced. Other growth factors such as IGF and insulin, can also modulate TOR activity. TORC1 is also sensitive to stress such as high temperature, hydrogen peroxide, and osmotic stress -all of which reduce or inactive TORC1.

TOR Signaling and Dietary Restriction

Dietary restriction (DR) is a commonly known way to slow aging across multiple species. DR not only slow the progression of many age related diseases, but it can also reduce or prevent cancer growth, neurodegeneration, and cardiovascular disease. TORC1 is thought to play a major role in the beneficial effects of DR.

In the genetically modified long lived Ames dwarf mouse, data support reduced TOR activity as a major factor in their long life span. Even non-modified mice administrated rapamycin in middle age saw a positive effect on life span.

Strong TORC1 inhibition early in life often yields damaging or fatal results, but TORC1 inhibition during adulthood can have the opposite effect and actually extend life.

Mediators of TORC1

Reduced protein synthesis as a result of inhibited TOR activity is one of the major factors in increasing life span across species. Restriction of dietary protein is known to have beneficial effects on life span, which is thought to be a result of reduced TOR activity due to reduced amino acid availability.

Also, the activation of S6 Kinase (a downstream process of TOR signaling) modulates protein synthesis and the inhibition of S6K has recently been found to also extend life in some species. Interestingly, female (but not male mice) lacking S6K have been observed to have longer life spans suggesting there may be a gender related component to TOR signaling and lifespan.

Final Thoughts:

Extensive evidence shows the nutrient and stress sensing of the TOR singling network as a major factor in  mediating responses to dietary restriction. Results indicate reduced TOR signaling works to extend life span. This information could lead to the development of “anti-aging” drugs.

Future work will include further examination of TOR signaling and DR as an aging modulator in a variety of species, and will hopefully elucidate the link between diet and age-related diseases.

Neat diagram that I don't have access to. Bah.

CONCLUSIONS: Considering the role of caloric restriction in increasing the intestinal uptake of carnitine, the results suggest that oral L-carnitine administration, when associated with a hypocaloric feeding regimen, improves insulin resistance and may represent an adjunctive treatment for IFG and DM-2.
  

Influence of a five-day vegetarian diet on urinary levels of antibiotics and phthalate metabolites: A pilot study with “TempleStay” participants

Antibiotic use is widespread in the animal farming industry, human exposure to such compounds can come through water source contamination and ingestion of animal products (negating the prescription antibiotics). Detecting the major sources for unintended human antibiotic exposure is critical due to antibiotic resistance and other adverse drug interactions.

Also, phthalates are a pervasive environmental contaminates with one major source of human exposure being diet, but these chemicals are also present in many products we use. In the CNN article, “5 Toxics that are everywhere: Protect yourself“, phthalates are the second toxin listed and they report, “Virtually everyone is exposed to phthalates”.

I think the most interesting part of this study, besides the results of course, is that the people being tested only changed their diets for 5 days. Only 5 days. Do note this study was conducted in Korea, but livestock in the USA are definitely given antibiotics too. Also, in the paper is a comparison to levels seen in Korea, USA, and Germany for curious readers.

The three antibiotics tested for were: sulfamethazine (SMZ), trimethoprim (TMP), and enrofloxacin (EFX). Four phthalates often reported in human samples were also testes for; these include: diethyl phthalate (DEP), di-n-butyl phthalate (DnBP), di-isobutyl phtalate (DiBP), and di(2-ethyl-hexyl) phalate (DEHP). A total of 25 participants (16 M, 9F) completed a 5-day vegetarian program, and levels of these antibiotics and phthalates were measured before and after the 5 day diet.

Typical Tap Water and Meat Consumption of Participants Before Diet

Antibiotics:

All 3 antibiotics were measured in the urine prior to the diet, although none were over the acceptable limit. Levels of all three antibiotics were lower after the diet, with some people reporting significant drops in certain antibiotic levels. Take a look at the numbers below:

Phthalates:

The phthalates measured before the diet were notably higher than the values often seen in the US general population, researchers noted, but some variations in the levels are present. Also, while diet is one major route of phthalate exposure, house dust, personal care products, and medications are also exposure sources in humans. So, some differences seen in reported levels for different countries could be explained by different common mechanisms of exposure.Below is the before and after measurements of phthalates for the 25 participants.

Oxidative Stress:

The researchers also measured the concentration of a urinary bio-marker for oxidative stress before and after the program, and found significant differences in the before and after values. Graph below:

Conclusion:

Based on the finding from this 5-day study, the researchers conclude that even a short-term dietary shift to vegetarianism can reduce dietary exposure to antibiotics and phthalates in the general population. In addition, oxidative stress levels were also seen to decrease.