In this week’s blog
on my homepage, I discussed the current obesity epidemic of our nation, how
children are being effected, and why getting fat is related to more than just a
“food input-output” issue. In this blog, I want to share with you some recent
studies that are further debunking the “calorie myth.”
Toxic Fat
Have
you heard of the term, “obsegenes?” It’s a word used to describe the connection
between toxic exposure and obesity. According to a 2012 study in Environmental Health Perspectives:
Obesity is
rising steadily around the world. Convincing evidence suggests that diet and
activity level are not the only factors in this trend–chemical “obesogens” may
alter human metabolism and predispose some people to gain weight. Fetal and
early-life exposures to certain obesogens may alter some individuals’
metabolism and fat-cell makeup for life. Other obesogenic effects are linked to
adulthood exposures.
This
term encompasses a broad array of chemicals which include pesticides, cigarette
smoke, and endocrine disruptors, such as bisphenols which are found in plastics.
Furthermore, the article points to a specific chemical, PFOA (perfluorooctanoic
acid):
Still another
widespread obesogen is perfluorooctanoic acid (PFOA), a potential endocrine
disruptor and known PPARγ agonist.42 “Pretty
much everyone in the U.S. has it in their blood, kids having higher levels than
adults, probably because of their habits. They crawl on carpets, on furniture,
and put things in their mouth more often,“
explains NIEHS biologist Suzanne Fenton. PFOA is a surfactant used for
reduction of friction, and it is also used in nonstick cookware, Gore-Tex™
waterproof clothing, Scotchgard™ stain repellent on carpeting, mattresses, and
microwavable food items. In 2005 DuPont settled a class-action lawsuit for
$107.6 million after its factory outside Parkersburg, West Virginia, tainted
nearby drinking water supplies with PFOA.43 In December 2011 an independent
science panel found the first “probable link” between PFOA and a human health
outcome, pregnancy-induced hypertension44 (for more information, see
“Pregnancy-Induced Hypertension ‘Probably Linked’ to PFOA Contamination,” p.
A59 this issue45).
Fenton
studied how PFOA levels similar to those in the tainted drinking water affected
the hormone levels and weight of rodent offspring exposed in utero.46 “We gave
pregnant mice PFOA only during pregnancy. It has a long half-life, so it hangs
around during lactation and gets delivered in milk to babies,” Fenton says.
“Once the offspring reached adulthood, they became obese, reaching
significantly higher weight levels than controls.”
Exposed
offspring also had elevated levels of leptin, a hormone secreted by adipose
tissue that affects appetite and metabolism. Leptin normally suppresses
appetite, but obese people and animals have elevated leptin levels, leading
researchers to suspect the brain can become resistant to its effects.47 Fenton
did not observe weight gain when mice were exposed to PFOA as adults, although
her team did find abnormalities in the uterus and mammary gland in exposed
adults.
Recently,
another study provided further evidence of PFOA exposure prenatally and
childhood weight. As reported by Health
Day:
A study of
more than 200 Cincinnati households finds that the children of mothers who
experienced higher levels of exposure to perfluorooctanoic acid (PFOA) while
pregnant had higher body fat and faster weight gain through age 8. The
participants live downstream from a chemical plant that used PFOA.
Interestingly,
chemicals could also impact our microbiome, and this can make us fat as well.
Belly Bugs
and Big Bellies
A
new study released this month reported on the mechanisms in how antibiotics
effect our microbiome. The study reported the following when using a mouse
model:
We found that
most antibiotic-induced alterations in the gut can be explained by three
factors: depletion of the microbiota; direct effects of antibiotics on host
tissues and the effects of remaining antibiotic-resistant microbes. Normal
microbiota depletion mostly led to downregulation of different aspects of
immunity. The two other factors (antibiotic direct effects on host tissues and
antibiotic-resistant microbes) primarily inhibited mitochondrial gene
expression and amounts of active mitochondria, increasing epithelial cell
death. By reconstructing and analysing the transkingdom network, we discovered
that these toxic effects were mediated by virulence/quorum sensing in
antibiotic-resistant bacteria, a finding further validated using in vitro
experiments.
These
little one trillion critters that line our insides, skin, and form our own
unique microbial
cloud
have so
many roles. These include: vitamin production, immune modulation,
cardiovascular health, mood and behavior effects, blood sugar balance,
digestion, skin health, liver health, hormonal balance, and more. This may be
why it was recently found that probiotics given to an infant’s feeding during
the first month was associated with decreased risk of type one diabetes in
genetically susceptible little ones.
So
it makes sense that antibiotics are also linked to weight gain in children. A
recent October 2015 study reported the following:
Results- Among 142 824 children under care
in the prior year, a reversible association was observed and this short-term
BMI gain was modified by age (P<0.001);
effect size peaked in mid-teen years. A persistent association was observed and
this association was stronger with increasing age (P<0.001). The addition of the progressive association among
children with at least three BMIs (n=79 752) revealed that
higher cumulative orders were associated with progressive weight gain; this did
not vary by age. Among children with an antibiotic order in the prior year and
at least seven lifetime orders, antibiotics (all classes combined) were
associated with an average weight gain of approximately 1.4 kg at age 15 years.
When antibiotic classes were evaluated separately, the largest weight gain at
15 years was associated with macrolide use.
Conclusions-We found evidence of
reversible, persistent, and progressive effects of antibiotic use on BMI
trajectories, with different effects by age, among mainly healthy children. The
results suggest that antibiotic use may influence weight gain throughout
childhood and not just during the earliest years as has been the primary focus
of most prior studies.
There’s
More
In order to really address the obesity epidemic, we
need to look for the root causes. Obesity is an effect of various factors includingfood quality,
stress control, hormonal balance, digestive function, activity, genetics,
gender (males and females have different responses to foods and exercise),
toxin exposures, neurotransmitter balance, and sleep. If diet and
exercise aren’t working for optimal weight, a naturopathic and/or functional
medicine doctor can help you navigate the weight loss maze.
Sources:
Holtcamp W. Obesogens: An
Environmental Link to Obesity. Environmental Health Perspectives.
2012;120(2):a62-a68. doi:10.1289/ehp.120-a62.
Orenstein
D. PFOA exposure in utero linked to child adiposity and faster BMI gain. Brown
University. November 11, 2015. https://news.brown.edu/articles/2015/11/adiposity
National
Institute of Environmental Health Sciences, Division of Extramural Research and
Training, Cellular, Organs and Systems Pathobiology Branch: NATIONAL ADVISORY
ENVIRONMENTAL
HEALTH SCIENCES COUNCIL. February 15-16, 2012. Concept Clearance: Microbiome/Environment
Interactions. Available at: https://www.niehs.nih.gov/news/newsletter/2012/4/science-microbiome/file64371_508.pdf
Morgun
A, Dzutsev A, Dong X, Greer RL, Sexton J, Ravel J, Schuster M, Hsiao W,
Matzinger P, Schulzhenko N. Uncovering effects of antibiotics on the host and
microbiota using transkingdom gene networks. Gut. 2015 Nov;64(11):1732-43. doi: 10.1136/gutjnl-2014-308820.
Gordon
S. Newborn Probiotic Use Tied to Lower Risk of Type 1 Diabetes. Health Day.
November 11, 2015.
Schwartz BS, Pollak J,
Bailey-Davis L, et al. Antibiotic use and childhood body mass index
trajectory.International Journal of Obesity. 21 October 2015;
doi: 10.1038/ijo.2015.218.
