I had
seen the previous incarnation of this study (1) a few years ago, so when
I saw the follow up study on the physiology feeds the other night, I
thought ‘Meh’ and wasn’t going to write about it. But yesterday
as soon as the media got their indelicate mitts upon it and spun up
headlines such as ‘Omega 3 Raise Risks of Prostate Cancer’, I received a
number of queries from concerned folk. So let’s take a look at this in a
less tabloid-esque sensationalistic manner.
The first and most
important take-away is that the study (2), despite what the media and
sadly one of the research team suggests, does not, in fact cannot, make
this definite claim. The study is based on a type of statistical science
what is known as epidemiology. Epidemiological studies look at patterns
and trends to begin to seek out links between factors. In the right
hands this can be a very powerful tool, which can help us find which
areas to focus upon and investigate further with more specific and
generally more expensive methods. It does have its problems though.
A basic example of this problem can be though of as thus:
In the summer time, more people suffer from sunburns.
Ice-cream sales increase in the summer time.
From this could we conclude that: Ice-cream causes sun-burn?
And this is the problem. The idea that because two factors ‘sun-burn’
and ‘Ice-cream’ happen to occur at the same time, doesn’t mean that one
necessarily ‘causes’ the other. In this case the forgotten factor was
the sun. There’s a very simple, but underappreciated maxim that says
‘Correlation doesn’t imply causation’. That is, just because there is a
link between factors doesn’t mean that one factor leads onto the other
factor. It ‘may’ but that is why further studies need to be done
accounting for all of the factors.
This current study suggests
that there is a link between high plasma omega 3 and the more aggressive
subset of prostate cancer. Now ‘link’ at this stage, refers to a
correlation i.e. Ice-cream, not a ‘causation’, so unlike the media let’s
not jump the gun.
This correlation could be because as the
paper suggests (I’ll cover one of the ways this ‘may’ happen in a later
Bite-size piece) that higher levels of omega 3 are influencing the
development (not initiating) of a more aggressive form of prostate
cancer, or, and this ‘may’ likely be the case, those who have prostate
cancer, especially those with the more aggressive subset have higher
levels of plasma omega 3. Although these appear to be the same
statement, they’re in fact totally different.
The study used
subjects whose ages ranged from 55-85, and this is important. By the age
of 50 almost all men have symptoms of prostate disease, which is
usually in the form of recurrent bouts of prostatitis (inflammation of
the prostate, often caused by infection), or as Benign Prostatic
Hyperplasia (BPH, overgrowth of the prostate gland, linked to
inflammation), some poor souls have both. By age 85, over 90% of men
have developed prostate cancer. I’m not suggesting a causal relationship
between the two, but there’s certainly a correlation between prior
inflammation in the prostate and the development of prostate cancer. We
also know that oxidative stress is part and parcel of the inflammatory
response, but we’ll come back to that in a moment as it muddies the
water slightly.
So we have a cohort in the right age range for
those who are displaying symptoms of some form of prostate disease,
whether it’s an ‘–itis’, benign hyperplasia or cancer. And we know that
the first two of these are intimately intertwined with inflammation, as
is the third. We also know that one of the most potent anti-inflammatory
substances we can get via nutrition is omega 3. So it doesn’t take much
thought, to see that those people who are displaying symptoms of
prostate disease, may have taken the route of upping their omega 3
consumption to reduce inflammation in hope of quenching the flames. And
the worse the symptoms the more someone is likely to do all they can to
combat them.
I say ‘all’, but that’s with some reservation.
Although omega 3 do have anti-inflammatory properties, they are far
outweighed by the excess amounts of omega 6 in the diet, which can be
both anti-, and pro-inflammatory. However, because of the way our
standard diets are set-up the pathway generally only runs down the
pro-inflammatory route. One of the key switches which select the pathway
that is used, is Insulin. There are many influences upon Insulin, but
the two biggies are high glycemic index carbohydrates and fructose.
Fructose can definitely be implicated, but again it will make the
picture too complicated. High glycemic index carbohydrates on the other
hand, are a little easier to associate (again correlation, not
causation). High GI carbohydrates are generally found as grains, which
just so happen to also be a rich source of omega 6, so we have a
foodstuff that loads the gun by providing the raw material for
pro-inflammatory substances and pulls the trigger by it’s production of
Insulin and thus the diverting of the cascade towards the
pro-inflammatory track.
Take a look at the newest rendition of
dietary advice (the EatWell Plate); one of the largest food groups
pushed by dietetics is grains and other high glycemic carbohydrates. The
current diet has a ratio of omega 6:3 of, on average, 15:1; to put this
in perspective our ancestor’s diets would’ve been closer to 1:1 - 1:2. A
gram or so of long chain omega 3 is a drop in the ocean compared to the
amounts of omega 6 we now consume. Maybe a better idea would be to
lower the intake of omega 6?
Think of it this way, if you
began running a tap and realised you had a blocked sink, would the
‘first’ thing you do be: a) call a plumber to come and fix the blockage,
or b) turn off the tap? Now replace the tap with omega 6, the blockage
with inflammation and the plumber with omega 3.
The study also
pointed to associations that the higher grade cases were more likely
to be being treated with finasteride (an alpha-5-reductase inhibitor
that prevents the conversion of testosterone into dihydrotestosterone)
and the lower grade case had less diabetes in their history. Another two
factors that point towards Insulin and inflammation as being pivotal.
So, when it comes to the study those who have the more aggressive form
of prostate cancer, and thus are more symptomatic, lo and behold, have
the highest plasma levels of omega 3. Just as an aside, the difference
between the two levels of omega 3 was about the difference between one
and two high omega 3 fish (salmon etc) meals per week. This situation
(taking in more omega 3 in an attempt to reduce inflammation) could be
one conclusion that can be drawn from the study. There are many others
which is why the media have done such a hatchet job on ‘reporting’ this
study.
The reason why omega 3’s are so potent is that they are
so biologically active, this is how they work in the body, they are
highly reactive, but it’s a double edged saw, as this activity also
allows them to be easily damaged. And this is why they are difficult to
get in the diet, as they can’t be implemented into processed foods
without becoming rancid (omega 6 are more robust and survive a lot
better in the manufacturing process), so people often use an omega 3
supplement. Companies who produce fish oil (the most widely used omega 3
supplement) have to protect the omega 3 in order to prevent them
becoming damaged. The way most companies do this is to encapsulate them,
thus protecting them from air (and thus oxygen), use opaque containers
to protect the oil from light, and if the company is good, keeps the
product refrigerated to prevent damage by heat. To up the ante, most
companies also add an anti-oxidant to the mix, and since fish oil is a
lipid, the most relevant type of anti-oxidant is lipid soluble and for
many reasons vitamin E fits the bill perfectly…almost.
The
study in question is part of larger project called the SELECT trial,
which had already suggested that vitamin E (the synthetic dl- racemic form) was associated with a 17%
increase in the risk of prostate cancer.(3) But as we know the Big G
likes to dwell in the details.
Vitamin E is one of the four
fat-soluble vitamins that cannot be made by the human body, so must be
ingested. Vitamin E is made by plants in eight different iso-forms
divided into two classes of four iso-forms. These usually come as mixed
tocopherols and tocotrienols in nature however most of the research is
on the D-alpha tocopherol form of natural vitamin E, which is the most
biologically active.
Synthetic vitamin E, is
DL-alpha-tocopherol, the laboratory produced form of the naturally
occurring, D-alpha tocopherol. Having both the D and the L isomers, and
this is key, renders it ineffective, as the L isomer does not occur in
nature, and our DNA does not recognise it.
Two of Vitamin E’s
functions are to 1) form part of the cellular membrane (membranes are
the surrounding seal of the cell) and defend it against oxidation, and
2) within the cell, and within its organelles such as the mitochondria,
vitamin E is the first line of defence against lipid peroxidation. This
is where the issue ‘may’ also be occurring.
The use of
synthetic vitamin E in the omega 3 supplements may be exposing the
membranes of the prostate cells to oxidative damage (by virtue of not
being the right tool for the job) and this may be compounded by the
incorporation of easily oxidised omega 3 into the membrane (which is
usually a good thing) allowing a chain reaction of oxidative damage to
occur. It ‘may’ also allow mitochondrial damage to proceed and this is a
biggie, since the mitochondria actually uses re-dox (which oxidation
forms the –ox part) pathways to dispose the body of damaged cells and
cell components.
This is only half of the problem, even if
you’re taking in sources (food or supplements) of natural forms of
vitamin E (which, by the way, are associated with lower incidence of
prostate cancer (4,5), taking single nutrients is never suggested by
anyone who knows anything about nutrition, doing so, especially with
what are termed ‘anti-oxidants’ may increase oxidative stress, even
using the natural forms that are supposed to be present in the Human
body. Nutrients, and especially anti-oxidants (more properly termed
‘re-dox agents’) always work in synergy. This is why a wide variety of
‘real’ food is promoted by those in the know, to hopefully obtain ‘all’
of the nutrients that work in cohesion.
There’s much more to
this story than the media have reported, but to discuss all of the
factors would become encyclopaedic. But here’s my take, like all disease
the incubation period is usually a long span of time, so the best time
to work on preventing disease is decades ago, the second best time is
today, before the rot sets in. Prostate cancer; like many diseases, are
mostly down to lifestyle factors. This is not a judgement it is merely a
fact. If you wish to avoid disease, clean up your lifestyle, and the
earlier, the better. Once disease is present and established, good
nutrition is definitely helpful; if not imperative, but sorry, it’s not a
cure. This is where we graciously ask the skilled and amazing health
care professionals to step in and use their methods of fighting back
diseased states. With their help, we can hopefully get another stab at
life. This is where nutrition can come back into play as the star
player, doing what it does best: slowly building a body that is
resilient to disease. Nutrients aren’t drugs, let’s not use them as
though they are.
References:
1- Brasky, TM et al.
Serum Phospholipid Fatty Acids and Prostate Cancer Risk: Results From
the Prostate Cancer Prevention Trial. Am J Epidemiol. 2011 June 15;
173(12): 1429–1439. Published online 2011 April 24. doi:
10.1093/aje/kwr027
2- Brasky, TM et al. Plasma Phospholipid
Fatty Acids and Prostate Cancer Risk in the SELECT Trial. JNCI J Natl
Cancer Inst (2013) doi: 10.1093/jnci/djt174. First published online:
July 10, 2013
3- Nicastro, HL and Dunn, BK. Selenium and
Prostate Cancer Prevention: Insights from the Selenium and Vitamin E
Cancer Prevention Trial (SELECT). Nutrients. 2013 April; 5(4):
1122–1148. Published online 2013 April 3. doi: 10.3390/nu5041122
4- Israel, K et al. RRR-α-tocopheryl succinate inhibits the
proliferation of human prostatic tumor cells with defective cell
cycle/differentiation pathways. Nutrition and Cancer, 1995;24:161-169
5- Eichholzer, M., Stähelin, H. B., Gey, K. F., Lüdin, E. and
Bernasconi, F. (1996), Prediction of male cancer mortality by plasma
levels of interacting vitamins: 17-year follow-up of the prospective
Basel study. Int. J. Cancer, 66: 145–150. doi:
10.1002/(SICI)1097-0215(19960410)66:2<145::AID-IJC1>3.0.CO;2-2
In the past few years the evidence has been mounting that fructose can
cause metabolic disturbance which may lead to development of metabolic
syndrome.
A new study has added
further weight behind this position, by suggesting that fructose can
promote rapid liver damage in certain diets that are high in this sugar.
The study used 10 middle-aged, normal weight monkeys who were fructose
naïve (never eaten fructose) and divided them into two groups based on
comparable body shapes and waist circumference. Over six weeks, one
group was fed a calorie-controlled diet consisting of 24 percent
fructose, while the control group was fed a calorie-controlled diet with
only a negligible amount of fructose, approximately 0.5 percent.
Each week during the study the research team weighed both groups and
measured their waist circumference, then adjusted the amount of food
provided to prevent weight gain. At the end of the study, the
researchers measured biomarkers of liver damage through blood samples
and examined what type of bacteria was in the intestine through faecal
samples and intestinal biopsies.
In the high-fructose group,
the researchers found that the type of intestinal bacteria hadn’t
changed, but that they were migrating to the liver more rapidly and
causing damage there. This is something that has been postulated in
Nutrition circles for a while now, that there seems to be something
about the high fructose levels that was causing the intestines to be
less protective than normal (Intestinal Permeability AKA ‘Leaky Gut’),
and consequently allowing the bacteria to leak out at a 30 percent
higher rate.
There are, however, a few caveats that have to be
taken into account. One is that, although the diets where similar in
carbohydrate, protein and fat levels, which was part of the control
methodology (to identify whether it was fructose alone, or in
combination with caloric excess that was causing the issue), the sources
providing these macronutrients where different, so this may have
influenced the findings. The second caveat, which the authors also
highlighted as a limitation of the study is that it only tested for
fructose and not dextrose (glucose). Fructose and dextrose are simple
sugars found naturally in plants, either individually or joined together
as sucrose i.e. table sugar.
The Authors studied fructose
because it is the most commonly added sugar in the American diet (where
the study took place), but based on their findings can’t say
conclusively that fructose caused the liver damage. They did suggest
though that high added sugars caused bacteria to exit the intestines, go
into the blood stream and damage the liver. They are planning a follow
up study to tease apart this detail.
I will go out on a limb
and suggest that the study will find that it ‘is’ the fructose that is
causing the damage. Not because fructose is evil, but because it is
doing what Nature intended it to do. The metabolic effects of fructose,
if you look at them with the right ‘per-spectacles’ is a genius design,
that probably kept us alive throughout our evolution. But when we took
the fructose out of context for example by refining the sugar out of
foods especially when we are using crops that we have purposely produced
to have a higher proportion of fructose i.e. High Fructose Corn Syrup,
then rather than a health promoting nutrient, we have a disease causing
agent.
I’ll keep you posted on the results of the study, if, and when it takes place
Reference:
Kavanagh, K et al. Dietary fructose induces endotoxemia and hepatic
injury in calorically controlled primates. Am J Clin Nutr August 2013,
doi: 10.3945/ajcn.112.057331
A recent review of the research involving the analogy between addictive
drugs, like cocaine, and hyper-palatable foods, notably those high in
added sugar, added more leverage to the idea that we are
living in what has been coined a ‘toxic food environment’. The food
environment is the physical and social surroundings that influence what
we eat. The ‘toxic’ part is how this current environment is making it
harder to choose healthy foods, and all too easy to choose unhealthy
food which then corrodes healthy lifestyles and promotes obesity. I have
written previously about this purposely manufactured design, which you
can find here: http://humanperformanceconsulting-uk.blogspot.co.uk/2011/12/celebrities-nibblys-pope-and-bear.html
The review found that the available evidence suggests that in humans,
sugar and sweetness can induce reward and craving that are comparable in
magnitude to those induced by addictive drugs. Although the authors of
the studies admit that this evidence is limited by the inherent
difficulty of comparing different types of rewards and psychological
experiences in humans, it is nevertheless supported by recent
experimental research on sugar and sweet reward in laboratory rats.
Overall, this research did reveal that sugar and sweet reward can not
only rival addictive drugs, like cocaine, but in fact on certain levels
be even more rewarding and attractive. On a neurobiological basis, the
neural effects of sugar and sweet reward appear to be more robust than
those of cocaine, which the authors suggest might possibly reflect past
selective evolutionary pressures for seeking and taking foods high in
sugar and energy density.
The authors of this review concluded
that the biological robustness in the neural effects of sugar and sweet
reward may be sufficient to explain why many people can have difficultly
in controlling the consumption of foods high in sugar when continuously
exposed to them.
Reference:
Ahmed, Serge H; Guillem,
Karine; Vandaele, Younaa. Sugar addiction: pushing the drug-sugar
analogy to the limit. Current Opinion in Clinical Nutrition &
Metabolic Care: July 2013 - Volume 16 - Issue 4 - p 434-439. doi:
10.1097/MCO.0b013e328361c8b8
Half of UK
population 'will get cancer in lifetime' was the headline emblazened
across the UK News feeds today (7th June 2013).
You can read the report by Macmillan Cancer Support here: http://www.macmillan.org.uk/Documents/AboutUs/Newsroom/Mortality-trends-2013-executive-summary-FINAL.pdf
I wrote about this last year in a post which you can find linked below.
I'm already part of the statistic, and as much as I love to be in good
company, in this circumstance I'm hoping you won't join me.
http://humanperformanceconsulting-uk.blogspot.co.uk/2012/02/keep-cancer-in-check.html
There is a gradual
shift in consciousness worldwide and this is very evident in the work of
many forward thinking and humble minds in science. As the veil of
hubris has been dropped, it is allowing us to discover, or rather
re-discover, the knowledge, understanding and wisdom of past great
minds such as Leonardo da Vinci, whose visionary understanding we are
only just beginning to appreciate. One such idea is summed up in his
statement ‘Realise that everything connects to everything else.’ With
the advent of Quantum theory we can see that on a micro- and macro-scale
this inter-connection certainly appears to be the case. Yet, in regards
to our bodies, the hubris of separation remains, both on a macro- and
micro-level. But times they are a-changing.
Less than a couple
of decades ago, most scientists wouldn’t have thought of body-fat as
anything more than a place where the body stores excess energy.
Subsequent research has found that it is much more than that; Body-fat
is now known to be a metabolically active 'endocrine' organ, capable of
secreting many molecular signals that communicate and influence the body
systems in their entirety, which when balanced support the functioning
of a healthy high performance body, but when out of balance lead to
dysfunction and disease.
Currently evidence is growing to
suggest that skeletal muscle also acts as an 'endocrine' organ and,
especially when exercised, could act as a mediator to many of the
signals originating from fat.
Within the last decade scientists have discovered that, like fat, muscles also secrete signaling molecules called ‘myokines.’
The discovery of myokines as protein messengers produced and secreted
by contracting muscle fibers is a paradigm shift, and like all good
science (which despite the common perception of it being a collection of
facts, is in fact a method to constantly challenge the status quo)
drastically alters the worldview in regards to metabolism and
physiology. This finding has provided a foundation to explain how
physical activity and muscle improve health and protect against chronic
disease.
Myokines are sent out by exercising muscle to relay
messages both locally within the muscle itself, as well as to other
organs throughout the body such as the brain, pancreas, liver, bone, and
adipose tissue. In some ways they mimic hormones, much like the earlier
discovered adipokines such as Leptin secreted from adipocytes (body fat
cells).
For the signals to have an effect, it is not
sufficient enough to simply produce them; the amplitude and the
frequency also have to be considered. Think of it in this way, from 1936
to 1955 the only television channel that you could view in the UK was
BBC One. They had the monopoly on the information broadcast (signals)
via a tele-visual medium. Beginning in 1955 ITV entered the foray, so
you now had two competing broadcasts each with their own specific remit.
Up until 1982 these two monoliths were the entirety for your
tele-visual (essentially) one-way communication. They would have shaped
and help form the world view of the viewers via their programming. Skip
to 2013, and the whole game has changed, no longer are these two
broadcasters the only players in the game, thus decreasing their
relative impact, despite having hugely increased absolute presence
(number of channels and extended viewing hours). And because of this,
the BBC is no longer the major (although still hugely influential)
provider of communiqué. This very same situation is reflected in the
body; it’s all about relatively dominant signals whether provided by
amplitude, frequency or a combination of the two.
When skeletal
muscle is a dominant organ over body fat – as found in lean adults,
where muscle can make up about 40 percent of body weight, the myokines
have a greater relative influence compared to the adipokines on many
different systems and metabolic processes in the body. Although the area
of myokine research is still in its birthing stages, the number of
myokines that have been identified and their roles are growing rapidly.
So far, studies have found that myokines influence muscle growth, fat
breakdown, insulin sensitivity, pancreas function, energy utilisation,
and risk of certain chronic diseases.
Two of the best studied
myokines to date are interleukin-6 (IL-6) and irisin, which the human
body makes a lot more of, when it moves more, such as in the performance
of physical activity, whether structured or not.
IL-6 was
first identified in 2000, and it was found that levels of it increased
100-fold after exercise (1). It was initially believed that this myokine
was an inflammatory mediator produced in response to muscle damage (1).
However, further studies revealed that although IL-6 does produce
inflammation when it is secreted by tissues such as immune cells, when
produced by skeletal muscle it acted conversely as an anti-inflammatory
agent.
Irisin is another myokine which has received much
attention within the last few years due to its ability to increase
energy expenditure. It does this through the development of a type of
body-fat called ‘brown fat’(2). I’ve previously written about this in a
number of articles, this HPC-UK Bitesize piece provides a link to the
core of them:
http://humanperformanceconsulting-uk.blogspot.co.uk/2013/02/get-hard.html
Physical activity has generally been viewed as a tool to balance energy
intake with expenditure and bring about weight loss, especially in the
latter half of the last century. However, we’ve known for quite a while
now, that thinking of physical activity in these terms is extremely
myopic. The influence of physical activity on energy expenditure is
obvious, the more you move, the more energy is used, but it is WAY
overstated. The real value of physical activity is not the increased
energy use during the sessions, nor is it really the slightly elevated
energy usage following exercise (EPOC – Excess Post-Exercise Oxygen
Consumption) which in the grander scheme of things are both relatively
minor, but something a lot more influential.
Physical activity
is one of the key stimuli that initiate a cascade that influences the
Human genome to express itself in support of a healthy and high
performance body and mind. Without that primary stimulus, your body, at
best, expresses itself as a merely sufficient version of your DNA to
exist, barely limping along. At worst it declines into disease and
death.
Far from the shallow view of muscles being simply a
veneer of vanity, science is proving that they are an integral part of
the whole, a part that you can choose to ignore; but do so at your
peril.
References:
1. Pedersen BK. Muscles and their myokines. J Exp Biol. 2011 Jan 15;214(Pt 2):337-46. doi: 10.1242/jeb.048074.
2. Boström P et al. A PGC1-α-dependent myokine that drives
brown-fat-like development of white fat and thermogenesis. Nature. 2012
Jan 11;481(7382):463-8. doi: 10.1038/nature10777.
Obesity is reaching epidemic levels in some parts of the world, and
scientists are teasing apart the details to understand why it is such a
persistent condition. A study in the
Journal of Biological Chemistry adds substantially to the story by the
discovery of a molecular chain of events in the brains of obese rats
that undermined their ability to suppress appetite and to increase
energy expenditure.
It's a vicious spiral, involving a
breakdown in how brain cells process key proteins that allows obesity to
promote further obesity. But researchers at Brown University found that
they could intervene to break that cycle by fixing the core
protein-processing problem.
We already know one mechanism in
which obesity perpetuates itself by causing resistance to leptin; a
hormone that signals the brain about the status of fat in the body.
However years ago senior author Eduardo A. Nillni, professor of medicine
at Brown University and a researcher at Rhode Island Hospital, observed
that after meals obese rats had a scarcity of another key
hormone—alpha-melanocyte stimulating hormone (a-MSH)—compared to rats of
normal weight.
Alpha-MSH has two jobs in parts of the
hypothalamus region of the brain. One is to suppress the activity of
food-seeking brain cells. The second is to signal other brain cells to
produce the hormone Thyrotropin-releasing hormone (TRH), which prompts
the thyroid gland to increase energy expenditure in the body. In the
obese rats alpha-MSH was low, despite an abundance of leptin and despite
normal levels of a very important protein called pro-opiomelanocortin
(POMC), which is a precursor to many vital chemicals in the body,
including a-MSH.
Since there was sufficient raw material for
a-MSH production and the enzymes for conversion were in place, the
researchers then smartly looked upstream of the process to see where, if
any, a limiting step occurred.
The research team fed one group
of rats a high-energy dense diet and fed others a normal diet for 12
weeks. The overfed rats developed the condition of ‘diet-induced
obesity.’ The team then studied the hormone levels and brain cell
physiology of the rats. They also tested their findings by experimenting
with the biochemistry of key individual cells in-vitro. They found that
in the obese rats the endoplasmic reticulum (ER), which is the part of
your cells that build your proteins, becomes stressed and overwhelmed.
The overloaded ER then failed to properly handle Prohormone Convertase 2
(PC2), which is a key enzyme in the synthesis of a-MSH.
The
PC2 levels they measured in obese rats, for example, were 53 percent
lower than in normal rats. Alpha-MSH peptides were also barely more than
half as abundant in obese rats as they were in healthy rats.
To confirm the findings, the researchers tested this concept further. In
additional experiments the researchers purposely induced stress in the
ER of a group of rats and found that there was a decrease in both PC2
and a-MSH. They also treated lean and obese rats for two days with a
chemical called Tauroursodeoxycholic acid (TUDCA), which is known to
alleviate ER stress. If ER stress was responsible for alpha-MSH
production problems, the researchers would see alpha-MSH recover in
obese rats treated with TUDCA. While TUDCA didn't increase alpha-MSH
production in normal rats, it increased it markedly in the obese rats.
The researchers also isolated neurons that produce PC2 and POMC and
pre-treated some with a similar chemical called 4-phenyl butyric acid
(PBA) that prevents ER stress. They left others untreated. They then
induced ER stress in all the cells. Under that ER stress, those that had
been pre-treated with PBA produced about twice as much PC2 as those
that had not.
The authors concluded that there is a direct
link between obesity and ER stress resulting in altered POMC processing,
which brings a new perspective of how ER stress can regulate energy
balance by altering POMC processing.
There are many factors
that are linked to ER stress, here are just a few: Glucose deprivation,
Calcium homeostasis disturbance, Hypoxia, Elevated homocysteine,
Pro-inflammatory mediators, ATP depletion, Excess Nitric Oxide, Alcohol
metabolism, Lp(a) cholesterol, Oxidised lipids, Oxidative stress, and
Insulin resistance.
Although this curtailed list still seems
like a lot of ground to cover, it’s actually really not. You can cover
all of those bases with a handful of relatively effortless lifestyle
modifications. And to really up the ante, if I’m correct, you may be
able to replicate the chemical intervention with a simple addition to
your meals which ties neatly into another groundbreaking study from a
few months back. Interesting times.
Reference:
Isin
Cakir, Nicole E. Cyr, Mario Perello, Bogdan Patedakis Litvinov, Amparo
Romero, Ronald C. Stuart, and Eduardo A. Nillni. Obesity Induces
Hypothalamic Endoplasmic Reticulum Stress and Impairs
Proopiomelanocortin (POMC) Post-translational Processing. J. Biol. Chem.
jbc.M113.475343. First Published on May 2, 2013,
doi:10.1074/jbc.M113.475343
Women's immune systems age more slowly than men's, and this slower
decline in a woman's immune system may contribute to women living longer
than men.
Researchers looked
at the blood of healthy volunteers in Japan, ranging in age between 20
and 90 years old; in both sexes the total number of white blood cells
per person decreased with age. The number of neutrophils decreased for
both sexes and lymphocytes decreased in men and increased in women.
Younger men generally have higher levels of lymphocytes than similarly
aged women, so as ageing happens, the number of lymphocytes becomes
comparable.
The study also suggests that the rate in decline
in T cells and B cells was slower for women than men. Both CD4+ T cells
and NK cells increased with age, and the rate of increase was higher in
women than men. Similarly an age-related decline in IL-6 and IL-10 was
worse in men. There was also an age-dependent decrease in red blood
cells for men but not women.
This difference in the ageing of
immune systems between men and women is one of many processes which
alter as we grow older, and the process of ageing is different for men
and women for many reasons; one of which is the sex hormones, which
affect the immune system, especially certain types of lymphocytes.
The lead researcher Prof Katsuiku Hirokawa postulates that because
people age at different rates a person's immunological parameters could
be used to provide an indication of their true biological age.
I’ve covered the main elements involved in ageing in previous posts which you can find by following the links provided here:
http://humanperformanceconsulting-uk.blogspot.co.uk/2011/05/elixir-of-life.html
http://humanperformanceconsulting-uk.blogspot.co.uk/2011/05/who-wants-to-live-forever.html
http://humanperformanceconsulting-uk.blogspot.co.uk/2011/09/hayflick-unlimited-part-1.html
http://humanperformanceconsulting-uk.blogspot.co.uk/2011/09/breath-of-fire.html
http://humanperformanceconsulting-uk.blogspot.co.uk/2011/09/in-pace-ut-sapiens-aptarit-idonea-bello.html
http://humanperformanceconsulting-uk.blogspot.co.uk/2011/10/demolition-man.html
http://humanperformanceconsulting-uk.blogspot.co.uk/2011/11/tame-flame.html
Reference:
Katsuiku Hirokawa, Masanori Utsuyama, Yoshio Hayashi, Masanobu
Kitagawa, Takashi Makinodan and Tamas Fulop. Slower immune system aging
in women versus men in the Japanese population. Immunity & Ageing,
2013; 10: 19
