In the
previous two pieces we saw that cellulite is a really a created term
propagated by the cosmetic industry to lull an ever increasing supply of
consumers into paying for products and services of dubious efficacy.
Even with the high-end treatments the change in appearance is a
temporary one at best, and at worst a causative agent in the aggravation
of the condition.
In this piece we’ll begin to look at the
conditions that contribute to the symptoms that are collectively called
cellulite and in understanding these factors try to divine the
interventions needed to modify the causes of the situation.
We
have already seen that the three main symptoms that in combination give
the bumpy appearance associated with cellulite are excess fat,
circulatory insufficiency, and connective tissue architecture.
Although it’s thought that cellulite is mainly a female concern, a
larger proportion of men than is readily apparent actually have a
condition similar to cellulite, its just better concealed. Part of the
cellulite condition is inadequate thickness of the skin, which is why
there are in fact many individuals (both male and female) that have all
of the other traits of cellulite, but because they have thicker skin,
the lumps and bumps aren’t as visible. This intervention (thickening the
skin) is actually one of the more successful interventions being
offered by the medical and cosmetic industries alike.
One of
the most effective methods of stimulating the body to remodel thicker
skin is through the use of Retin-A; and herein lies a sorry tale.
Retin-A works very effectively to remodel skin by removing damaged
protein structures, and stimulating the growth of new proteins to create
a more uniform and thicker skin. It was developed in the late 1960’s as
a treatment for skin conditions such as acne vulgaris and keratosis
pilaris (chicken skin). However, once Retin-A, which is a derivative of
vitamin A (retinol), was shown to have real world effect, it was
immediately seized by the pharmaceutical industry and is now a regulated
treatment. This is true of many effective treatments, once they show
real biological effect they are then usually re-classified as a drug and
subsequently tightly regulated. Sometimes this is a good thing as some
people really do need saving from themselves, sadly it does however
restrict access to the more level headed of us.
So for most of
us Retin-A is off the table but there are other chemicals that are
accessible which perform a similar function; these are the hydroxy acids
(alpha and beta). Hydroxy acids, like Retin-A, stimulate the growth of
new proteins within the skin to produce a thicker more even tone. As
suggested in the previous instalments, this isn’t an overnight effect,
both Retin-A and Hydroxy acids stimulate the remodelling of your skin,
but this is dependent upon physiological dynamics. The cells that make
up your skin take a minimum of two weeks to turnover (they’re in
constant flux, breaking down and re-building), but the change in each
cycle is miniscule, so it takes a number of these cycles to create an
appreciable effect. The remodelling process is reliant on the consistent
provision of beneficial nutrients, the right signals and the
minimisation of destructive stresses. Even with daily attention to
providing the right environment for optimal skin health it will take at
least 6-12 months to have any lasting effect. You have to grow a better
body.
Nutrition for skin health is beyond the scope of this
article, but here are a few tips to assist in the remodelling of skin
towards a thicker, more evenly toned expression.
First, you
need to wash, carefully. Keeping your skin clean is essential to
minimise the toxins we are bombarded with daily from stressing the skin
and causing an inflammatory condition which then prevents the effective
remodelling of skin as well as at the same time as highlighting the
hills and valleys due to fluid retention. However, over-zealous cleaning
is counter-productive as it removes the natural humectant coating
(moisture retaining substances) and disturbs the microbiome (bacteria)
that maintains skin health. Excessive cleaning may in fact contribute to
the appearance of cellulite by removing these two key features of the
skin environment. Use gentle cleansers and do not use regular soap.
As well as maintaining skin hygiene, you can assist the process by
gentle exfoliation. Uneven skin, like local inflammation, highlights the
lumpy appearance of cellulite. Regular exfoliation to smooth out the
skin will slightly reduce the appearance of cellulite, although it is a
mostly cosmetic effect. It is however necessary to remove the flaky skin
cells which contribute to irregular texture and also provides a ready
source of nutrition (the skin cells) for specific bacteria that
contributes to poor skin health. Again like cleansing, you need to be
gentle and consistent, a few times per week is more than sufficient. The
key is to encourage a better environment for healthy renewal, if you
try to push it, however, the body will push back, often with results
being the opposite for which you’d hoped.
Once you’ve thrown
out the surface garbage, you can then attend to the task of remodelling
the real skin structure. If you have access and you can afford it, then
you can enlist the aid of a medical specialist hopefully well versed in
dermatology who can provide you with an individual protocol for the use
of Retin-A. The rest of us from more meagre holdings have to rely upon
more accessible chemicals to assist us in stimulating an increased
turnover of the proteins in the skin, which as we saw above were the
hydroxy acids. There are three common hydroxy acids, lactic acid
(alpha-) and glycolic acid (alpha-), which are both water soluble, and
salicylic acid (beta-) which is lipid soluble. The lipid soluble
beta-hydroxy acid is especially beneficial as it can penetrate through
the fatty structures in the skin, so has a more widespread effect than
the alpha-hydroxy acids. Daily and judicial use of these chemicals will
gradually change the structure of the skin to a more healthy and
abundant landscape (i.e. thicker and more uniform), but keep in mind
that this will take a year or so for permanent (-ish) effect.
The final factor (in our small summary) that will vastly improve the
health of your skin and improve the appearance of cellulite is the
hydration status of your skin. Like the rest of your body, the skin is
mostly water. However, due to its direct interaction with the
environment, it has to deal with multiple stressors many of which cause
it to dry out. I’ve covered previously how the hydration status of the
cells in the body is in itself a potent signal that then dictates
various cascades to either promote certain biochemical pathways or block
them.
Most of the topical cellulite treatments simply work by
causing the retention of water in the skin. This assists in the healthy
turnover of the skin and temporarily smoothes out the skin, giving the
illusion of reduced cellulite. One of the key ingredients that can
achieve this is hyaluronic acid which helps to increase the skin's
natural elastin levels. Hyaluronic acid does this by absorbing fairly
large amounts of water which then supports the elasticity and youthful
appearance of skin.
Performed regularly these activities will
go some way to providing the skin with the correct signals to stimulate a
thicker and more even skin texture and tone which in part will reduce
the appearance of cellulite. This in itself is really only a cosmetic
effect as we have done nothing to address the underlying connective
tissue structure, nor the excess adiposity that is creating the pressure
upon the collagen matrix. That is what we will address in the next
piece in this series, as they are both fairly involved scenarios.
In the previous
instalment (Peeling Back The Truth of Cellulite) we saw that cellulite
is not truly a real discrete thing. It is however a perfect storm of
contributory factors which lead to three primary manifestations:
abnormal connective tissue, adipose excess and dysfunction, and local
circulatory insufficiency. So to permanently reduce cellulite, all three
of these symptoms, and more pertinently, their causes need to be
addressed. The majority of treatments touted as cellulite ‘cures’, not
only fail to use that simple premise, but by virtue of the mechanisms of
some of the treatments (usually the ‘premium’ modalities) often
exacerbate the issue in the long run.
The following are a few of the current treatments that propose to cure cellulite:
Laser
The use of laser therapy comes in a few different flavours, but the
versions that are sufficiently powerful are obviously regulated and only
available via medical professionals. The low power laser therapies
offered by your local beauty therapist have an effect by a totally
different mechanism.
The current professional therapies use a
cannula with an integrated laser that is used to disrupt the fat cells
and collagen fibers. This disruption will obviously change the structure
in the area and temporarily improve the appearance of cellulite.
However, it doesn’t change the environment that caused the cellulite to
appear in the first place, so can’t prevent the re-appearance of the
abnormal infrastructure. And because the treatment causes very rapid
destruction of the tissues, it will feed into the chronic inflammatory
cascade that is a prevalent factor in the cellulite condition. So it’s
not unfeasible that the use of this invasive and highly destructive
process could actually accelerate the condition. Of course this won’t be
evident in the first 12 months or so as it will take time to re-grow
the tissues, but once it does, the likelihood is that the situation will
be even more aggressive than before the treatment.
Acoustic Wave
Therapies based on acoustics use a high energy wave, it is
proposed, to disrupt the adipose tissue that is pushing through the
connective tissue matrix. There is limited evidence that this occurs,
but even so even if it did work, like the laser therapy it doesn’t
address the cause of the cellulite, and again may actually act as a
promoter of subsequent development.
Mesotherapy
Mesotherapy uses injections to ‘dissolve’ the fat cells through the use
of many different chemicals. The chemical used depends on the
practitioner. Although the word ‘dissolve’ is often used for marketing
purposes, the injections aim to cause cellular apoptosis (cell death) in
the fatty tissue. If the treatment is successful in achieving what it
suggests, it too will suffer from the same issues as the above two
therapies. Tissues don’t simply dissolve and flush out of the body, it
requires a huge local and systemic immune response to remove the debris,
which as previously suggested will feed back into the process that
promoted and maintained the development of cellulite.
Thermotherapy
Like the laser therapies there are a few different versions of this,
the premium treatments again need to be performed by a medical
professional. These premium treatments use radio-frequencies to target
the underlying structures and generate high levels of local heating
which like the above therapies cause cellular apoptosis and the
resultant widespread debris caused by the death of cells in the tissues.
There are side-effects of the treatment that do improve, temporarily,
the cosmetic appearance of cellulite.
There are many other
therapies that also claim to reduce cellulite such as Iontophoresis that
uses galvanic currents to increase the permeability of the skin in an
attempt to pass various substances through to the lower layers, or
Electrophoresis that creates an electrical field that is suggested to
alter the flow of nutrients in the area to increase the structure of the
connective tissue to a more normal pattern and also assist in lipolysis
(fat breakdown). Neither treatment has shown conclusive evidence of
improvements in studies on cellulite.
In the more accessible
treatments available to the public such as low level laser,
iontophoresis, lymphatic drainage, wraps, and pressotherapy, the one
common factor (whether overtly evident or not) is massage. Part of the
issue with cellulite especially in the higher stages is localised oedema
(swelling or fluid retention) which is a symptom of the inflammatory
environment and various mechanical factors. The use of massage
temporarily shifts the fluid out of the compartment and reduces the
pressure being placed on the connective tissue matrix, giving the
appearance of reduced cellulite. Given a few days or often hours, the
osmotic pressures normalise and the fluid re-enters the area, and you’re
back to square one. This is mostly how the crèmes and lotions ‘work’
too, via the fact that during application you are giving the area a
daily massage. Massage does assist in the treatment of cellulite, and is
a helpful part of the equation, but don’t confuse the temporary
appearance change caused by some of the more aggressive treatments with
anything being done to the actual structures. The main benefit of
massage is to assist in the circulatory flow in the region, which needs
to be a continual presence, not a once or twice a week temporary
cosmetic illusion.
The above treatments cannot result in
permanent alterations of the presence of cellulite, simply because they
treat, with various efficacy, the symptoms of cellulite whether
individual or in combination. They do nothing to address the underlying
causes and will therefore allow the situation to continue, or as we have
seen may actually intensify the progression of cellulite. In the next
post we’ll look at how cellulite develops and once we’ve understood this
environment we can then consider solutions to mitigate and even reverse
the condition
Orange Peel, Mattress Skin, Cottage Cheese, Bubble Wrap are just a few
of the words used to describe cellulite; the bumpy appearance some women
and men exhibit especially in the abdomen and upper thighs.
Looking on Google, the search term ‘cellulite’ is an annual favourite,
especially in the months leading up to summer. Despite the apparent
widespread acceptance as a real phenomenon, it is not actually an
acknowledged term in medicine. Which in their (the medical orthodoxy)
defence, is actually closer to the truth than marketers would have you
believe. At one end of the scale the medical establishment, if asked,
will inform you that ‘cellulite’ is simply body-fat. At the other end of
the scale the marketers, of endless products and treatments, will have
you believe that cellulite is a discrete type of tissue that can only be
removed by use of this newly discovered secret and proprietary
mechanism. The ‘discreteness’, of course, is different in each case
depending on what and how the product or treatment they hope to sell you
works. The truth, as you’ll see, lies somewhere in between these two;
but very much closer to the orthodox medical end of the spectrum.
The term ‘cellulite’ was coined in the 1920’s but didn’t really become a
household term until the 1970’s when cosmetic companies got hold of it
and used it in combination with the twin darlings of marketing ‘vanity’
and ‘fear’, to sell dubious crèmes and lotions, that cost pennies to
make and that sold at a premium. As we’ll see, although the application
of these crèmes does temporarily (hours) reduce the appearance (not the
real structure) of cellulite, use of these crèmes may actually hasten
its development.
Body-fat ‘is’ a major player in cellulite, the
medical establishment are absolutely correct on that, but, that’s not
where the story ends. Cellulite is not simply caused by body-fat alone,
it’s a combination of specific local structures caused by the interplay
of energetics, hormones and other physiological factors that all
contribute to this condition. In simple terms it’s excessively full fat
cells protruding through the mesh of connective tissue in the skin
above.
Before we get into the details of the conditions that
contribute to cellulite (in successive posts) or the current
‘treatments’ purported as cures (next post), I just want to quickly
cover a very important point to help you navigate the disingenuous
market-place to save you from being hoodwinked. Because of the
physiological conditions that contribute to cellulite it takes at least 6
months of daily interventions to change. Anyone claiming to remove
cellulite in a few treatments is not quite telling you the truth,
whether intentionally or just through their own ignorance. And because
of these specific physiological conditions, no degree of external (or
internal, as you’ll see in the next post) prodding, poking, lasering,
suction or wrapping will amount to anything permanent.
Cellulite is relatively simple to fix, but it does take a few lifestyle
changes to do it properly. A saying I always bear in mind when
considering my actions is ‘If you haven’t got the time to do it right,
when will you find the time to do it over’.
Do it right, once.
The everyday
language we repeatedly use shapes our behaviour. Habitually using the
right words spoken in the right way can bring us compassion, respect and
strength in life. The wrong words can all too easily bring us dislike,
disrespect and instability. To improve our likelihood of achieving our
goals and aspirations we have to improve what we say, not only to others
but also to ourselves.
Whenever we feel sensations such as joy
or sadness, those sensations are weighted emotionally by the word
labels we attach to them. The labels that we attach to our experience
become our thoughts and our memories of that experience. The phrase ‘I’m
enraged’ leaves a very different emotional and biochemical memory
pattern than does ‘I’m a bit miffed by that.’
Habitual
self-language patterns are often not recognised, so people do not
realise their influence. However you can begin to appreciate how they
(words) affect you when you consider how we are spoken to by others. If
somebody told you ‘I think you’re mistaken’, the phrase doesn’t create
the same level of emotional response as somebody saying ‘You’re wrong’,
and it certainly has nowhere near the same emotional response than if
they had said, ‘You’re a damn liar’. All three phrases are essentially
saying the same thing, but the level of emotional attachment is orders
of magnitude different in each case.
A new study has shown how words in our environment, even on an unconscious level, can dramatically alter your behaviour
Inhibitory self control such as not picking up a cigarette, not having a
second drink, not spending when we should be saving, can operate
without our awareness or intention.
Researchers at
the University of Pennsylvania’s Annenberg School for Communication and
the University of Illinois (Urbana-Champaign) demonstrated through
neuroscience research that inaction-related words in our environment can
unconsciously influence our self-control. Mindlessly eating nibbly’s at
a party or stopping ourselves from over-indulging may seem impossible
without a deliberate, conscious effort. However, the research indicates
that overhearing specific language, even in a completely unrelated
conversation, saying something as simple as ‘calm down’ might trigger us
to curtail our junkie-like biscuit eating frenzy without us even
realising it.
Subjects in the study completed a
task where they were given instructions to press a computer key when
they saw the letter ‘X’ on the computer screen, or not press a key when
they saw the letter ‘Y.’ Their actions were affected by subliminal
messages flashing rapidly on the screen (too fast to be consciously
seen). Action messages such as ‘run,’ ‘go,’ ‘move,’ ‘hit,’ and ‘start’
alternated with inaction messages ‘still,’ ‘sit,’ ‘rest,’ ‘calm,’ and
‘stop’ and nonsense words ‘rnu,’ or ‘tsi’. During the test the subjects
wore an EEG (electroencephalogram) device to measure brain activity.
The test was cleverly set-up so that the action or inaction messages
had nothing to do with the actions or inactions volunteers were doing,
yet the researchers found that the action/inaction words had a definite
effect on the volunteers’ brain activity. Unconscious exposure to
inaction messages increased the activity of the brain’s self-control
processes, whereas unconscious exposure to action messages decreased
this same activity.
The researchers said ‘Many
important behaviours such as weight loss, giving up smoking, and saving
money involve a lot of self-control’. ‘While many psychological theories
state that actions can be initiated automatically, with little or no
conscious effort, these same theories view inhibition as an effortful,
consciously controlled process. Although reaching for that cookie
doesn’t require much thought, putting it back on the plate seems to
require a deliberate, conscious intervention. Our research challenges
the long-held assumption that inhibition processes require conscious
control to operate.’
This study further reinforces the concept
of words having power; regardless of whether the interaction is on a
conscious or an unconscious level.
A good idea (in general,
not just in respect of this premise) is to expand your vocabulary. Find a
new word to displace the words you usually use when you encounter a
situation. Use the new words regularly to heighten the emotional
intensity for the positive aspects of your life, and most importantly
use new lower impact words for the negative experiences you encounter.
Gradually improving your habitual vocabulary is a wise investment.
You’ll rapidly alter how you think, how you feel, and how you behave.
Without question there will still be times, for example, when we feel
justified in being incensed, but by controlling your language patterns,
you will be able to control your emotions to direct and utilise them to
better effect. Your choice.
Reference:
Justin Hepler,
Dolores Albarracin. Complete unconscious control: Using (in)action
primes to demonstrate completely unconscious activation of inhibitory
control mechanisms. Cognition, 2013; 128 (3): 271 DOI:
10.1016/j.cognition.2013.04.012
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
