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
After weight loss, total energy expenditure—in particular, energy
expenditure at low levels of physical activity—is disproportionately
lower than predicted by actual changes in body weight and
composition. This is known as adaptive thermogenesis.* A key issue is
whether this reduction, which predisposes towards weight regain,
persists over time.
The increasing prevalence of obesity and
its co-morbidities reflects the interaction of genes that favour the
storage of excess energy as fat with an environment that provides ad
libitum availability of energy-dense foods and encourages an
increasingly sedentary lifestyle. Although weight reduction performed in
the typical manner (Calorie restriction) is difficult in and of itself,
anyone who has ever lost weight will confirm that it is much harder to
keep the weight off once it has been lost.
The over 80%
(thought to be closer to 95-98%) recidivism rate to pre-weight loss
levels of body fatness after otherwise ‘successful’ weight loss is due
to the coordinate actions of metabolic, behavioural, neuro-endocrine and
autonomic responses designed to maintain body energy stores (fat) at a
central nervous system-defined 'ideal'. This adaptive thermogenesis
creates the ideal situation for weight regain and is evident in both
lean and obese individuals attempting to sustain reduced body weights.
The multiple systems regulating energy stores and opposing the
maintenance of a reduced body weight illustrate that body energy stores
in general and obesity in particular are actively 'defended' by
interlocking bio-energetic and neurobiological physiologies.
A recent study aimed to investigate whether adaptive thermogenesis is sustained during weight maintenance after weight loss.
The study was performed using 22 men and 69 women (average age of 40
with a body mass index of 31.9) who followed a very-low-energy diet for 8
weeks, followed by a 44-week period of weight maintenance. The subjects
were assessed for body-composition and metabolic rate. Measurements
took place before the diet and at 8, 20, and 52 weeks after the start of
the diet.
The results demonstrated a reduction in metabolic
rate at the end of the dieting period (week 8 ) and this decrease was
sustained after 20 weeks and 52 weeks.
The authors concluded
that weight loss results in adaptive thermogenesis, and there is no
indication for a change in adaptive thermogenesis up to 1 year, when
weight loss is maintained.
Reference:
Stefan GJA
Camps, Sanne PM Verhoef, and Klaas R Westerterp. Weight loss, weight
maintenance, and adaptive thermogenesis. Am J Clin Nutr May 2013 97:
990-994.
* http://humanperformanceconsulting-uk.blogspot.co.uk/2012/01/ive-got-chills-theyre-multiplying.html
New research shows that growing up in areas where air pollution is
increased raises the risk of insulin resistance (the precursor to type
ii diabetes) in children.
Previous studies
have identified links between air pollution and other chronic
conditions such as cardiovascular and respiratory disease. However to
date, epidemiological studies that have examined associations between
long-term exposure to traffic-related air pollution and type ii diabetes
in adults have been inconsistent, and studies on insulin resistance in
children are sparse. Thus this new study sought to explore the possible
association between air pollution and insulin resistance in children.
Even though toxicity differs between air pollutants, they are all
considered potent oxidisers that act either directly on lipids and
proteins or indirectly through the activation of intracellular oxidant
pathways. Oxidative stress caused by exposure to air pollutants may
therefore play a role in the development of insulin resistance. In
addition, some studies have reported that short-term and long-term
increases in particulate matter and nitrogen dioxide (NO2) exposure lead
to elevated inflammatory biomarkers, another potential mechanism for
insulin resistance.
In this new study, fasting blood samples
were collected from 397 10-year-old children as part of a larger birth
cohort study. Individual-level exposures to traffic-related air
pollutants at birth address were estimated by analysing emission from
road traffic in the neighbourhood, population density and land use in
the area, and the association between air pollution and insulin
resistance was calculated using a model adjusted for several possible
confounders including socioeconomic status of the family, birth-weight,
pubertal status and BMI. Models were also further adjusted for
second-hand smoke exposure at home.
The researchers found that
in all crude and adjusted models, levels of insulin resistance were
greater in children with higher exposure to air pollution. Insulin
resistance increased by 17% for every 10.6 µg/m3 (2 standard deviations
from the mean) increase in ambient nitrogen dioxide (NO2) and 19% for
every 6 µg/m3 (2 SDs) increase in particulate matter of up to 10 μm in
diameter. Proximity to the nearest major road increased insulin
resistance by 7% per 500 metres. All the findings were statistically
significant.
Insulin resistance levels tended to increase with
increasing air pollution exposure, and this observation remained robust
after adjustment for several confounding factors, including
socioeconomic status, BMI and passive smoking.
Reference:
E. Thiering & J. Cyrys & J. Kratzsch & C. Meisinger &
B. Hoffmann & D. Berdel & A. von Berg & S. Koletzko &
C.-P. Bauer & J. Heinrich. Long-term exposure to traffic-related air
pollution and insulin resistance in children: results from the GINIplus
and LISAplus birth cohorts. Diabetologia. DOI 10.1007/s00125-013-2925-x
Having trouble falling or staying asleep? According to a new study led
by a team of researchers at the Johns Hopkins Bloomberg School of Public
Health, insomnia may be an important indicator of future
hospitalisation among middle-aged and older adults. They examined the
association between insomnia and use of home healthcare services,
nursing homes and hospitalisation and found that insomnia symptoms
experienced by middle-aged and older adults were associated with greater
future use of costly health services.
The study used a large
representative sample of US middle-aged and older adults, and found that
individuals with a greater number of insomnia symptoms were more likely
to be hospitalised, and to use home healthcare services. Over 40
percent of the sample reported at least one insomnia symptom, consistent
with previous studies that showed insomnia to be very common in this
population. The authors suggest that if the association between insomnia
symptoms and health service utilisation is causal, the findings would
suggest that the prevention of insomnia could decrease health service
use by 6-14 percent in this population.
According to the
National Institutes of Health, insomnia is the most common sleep
complaint at any age and affects almost half of adults ages 60 and
older. Insomnia symptoms include difficulty falling asleep, staying
asleep, or both, and individuals with insomnia often report getting too
little sleep, having poor sleep quality and not feeling refreshed when
they wake up.
Lead author of the study, Christopher Kaufmann,
MHS, and his colleagues examined the association between insomnia
symptoms and reports of health service utilisation using data from the
Health and Retirement Study. Participants were asked how often they
experienced trouble falling asleep; trouble with waking up during the
night; trouble with waking up too early and not being able to fall
asleep again, and how often they felt rested when they woke up. The
researchers evaluated health care utilisation in 2006 and respondents
were asked questions about their use of several health services two
years later, including whether they were hospitalised, used home health
care services, or were placed in a nursing home. Participants'
demographic characteristics as well as current or previous medical
conditions were also recorded. The researchers found that there was a
statistically significant relationship between the report of insomnia
symptoms and the future use of costly health services. A relationship
was even found between insomnia symptoms and hospitalisation as well as
use of any of the three health services after accounting for common
medical conditions and elevated depressive symptoms.
The
results suggest that treating and carefully monitoring insomnia symptoms
in middle-aged and older adults might somewhat reduce the use of health
services and presumably the poor health outcomes that necessitate these
services.
Reference:
Kaufmann. C N et al. Insomnia
and Health Services Utilisation in Middle-Aged and Older Adults: Results
From the Health and Retirement Study. J Gerontol A Biol Sci Med Sci
(2013) doi: 10.1093/gerona/glt050
Despite the huge knowledge explosion we have had in the physiology
world in the last decade, especially since the human genome project
produced the genomic map, the mainstream ‘weight loss’ industry still
haven’t really changed their mantra of ‘Eat less’. I’ve shown previously
multiple ways why this doesn’t work as
advertised, in terms of actual fat lost (there is some temporary loss of
the fat droplet inside the fat cell, but plenty of muscle and
unfortunately for women bone loss too), nor does it cause a permanent
change to your physiology, especially the functioning of the fat cell
itself, so that you are able to maintain a lower fat body. Even if it
did work, a recent study has shown one of the mechanisms that makes it
difficult to achieve long term.
Oregon Research Institute (ORI)
senior scientist Eric Stice, Ph.D., and colleagues provide results in a
recent issue of NeuroImage that further our understanding of how and
why most weight loss diets fail and provide a description of the impact
of caloric restriction.
The study suggests that restricting
food intake increases the reward value of food, particularly
high-calorie, appetizing food, and that the more successful people are
at caloric-restriction dieting, the greater difficulty they will face in
maintaining the restriction. Additionally, abstaining from food intake
for longer durations of time also increases the reward value of food,
which may lead to poor food choices when the individual eventually does
eat.
The data suggests that elective caloric restriction
increases the degree to which brain regions implicated in reward
valuation and attention are activated by exposure to palatable foods.
Participants in the study were split into two groups (Study 1 n=34;
Study 2 n=51) who voluntarily restricted their caloric intake so as to
approximate what occurs with real-world dieters. Using brain imaging the
research team examined the responsivity of the subject’s attention and
reward regions of the brain to the individual's exposure to and imagined
intake of palatable foods, unpalatable foods, and glasses of water
shown in pictures. By including both pictures of palatable and
unpalatable foods, the team was able to determine whether degree of
"self-imposed" caloric deprivation correlated with hyper-responsivity of
attention and reward regions for palatable versus unpalatable foods.
The team also measured the subject’s neural responses to consumption
and anticipated consumption of a chocolate milkshake and a calorie-free
tasteless solution. The lead researcher Dr. Stice examined whether the
number of hours since last caloric intake (which varied from 3 to 22
hours) correlated with neural activation in response to receipt and
anticipated receipt of a palatable food. They also tested whether the
subject’s who were in a negative energy balance for a 2-week period
versus energy balance or a positive energy balance showed aberrant
neural response to food stimuli.
The research team concluded
that the implications of this imaging study suggest that if people want
to lose excess weight, it would be more effective to consume healthy,
lower energy dense foods during regular meals, rather than go for long
periods of time without any caloric intake.
Reference:
Eric Stice, Kyle Burger, Sonja Yokum. Caloric deprivation increases
responsivity of attention and reward brain regions to intake,
anticipated intake, and images of palatable foods. NeuroImage, 2013; 67:
322 DOI: 10.1016/j.neuroimage.2012.11.028
Ageing is a result of gradual and overall functional deteriorations
across the body. We have an idea about many of the processes involved,
however a recent study has postulated that a specific part of the brain
is central to the rate at which ageing occurs throughout the body.
This shouldn’t surprise anyone who has done the HPC-UK Lean for Life
program, as we discover throughout that the brain is the key player in
pretty much everything. This piece of research also wasn’t a surprise to
me, as I had learned this specific pathway of ageing described in the
study almost a decade ago.*
The part of the brain in question
is the hypothalamus, an almond-sized structure located deep within the
brain, which is known to have fundamental roles in growth, development,
reproduction, and metabolism. The lead researcher on the study, Dr. Cai,
suspected that the hypothalamus might also play a key role in ageing
through the influence it exerts throughout the body.
As people
age inflammation gradually increases in various tissues. We know that
inflammation is involved in various age-related diseases, such as
metabolic syndrome, cardiovascular disease, neurological disease and
many types of cancer. Over the past several years, Dr. Cai and his
research colleagues showed that inflammatory changes in the hypothalamus
can give rise to various components of metabolic syndrome (a
combination of health problems that can lead to, amongst a growing list,
heart disease and diabetes).
To find out how the
hypothalamus might affect ageing, Dr. Cai decided to study hypothalamic
inflammation by focusing on a protein complex called NF-κB (nuclear
factor kappa-light-chain-enhancer of activated B cells). Inflammation involves hundreds of molecules, but NF-κB is a key regulator of the cascade.
In the current study, Dr. Cai and his team demonstrated that activating
the NF-κB pathway in the hypothalamus of mice significantly accelerated
the development of aging, as shown by various physiological, cognitive,
and behavioral tests. This resulted in the mice showing a decrease in
muscle strength and size, in skin thickness, and in their ability to
learn -- all indicators of ageing. Activating this pathway promoted
systemic ageing that shortened the lifespan.
Conversely, Dr.
Cai and his group found that blocking the NF-κB pathway in the
hypothalamus of mouse brains slowed ageing and increased average
longevity by about 20 percent, compared to controls.
The
researchers also found that activating the NF-κB pathway in the
hypothalamus caused declines in levels of gonadotropin-releasing hormone
(GnRH), which is synthesized in the hypothalamus. Release of GnRH into
the blood is usually associated with reproduction. Suspecting that
reduced release of GnRH from the brain might contribute to whole-body
aging, the researchers increased levels of the hormone in the
hypothalamic ventricle of aged mice and discovered that the hormone
protected them from the impaired neurogenesis (the creation of new
neurons in the brain) associated with ageing. The aged mice who received
the daily GnRH augmentation for a prolonged period demonstrated
benefits that included the slowing of age-related cognitive decline,
probably via the result of neurogenesis.
Reference:
Guo Zhang, Juxue Li, Sudarshana Purkayastha, Yizhe Tang, Hai Zhang, Ye
Yin, Bo Li, Gang Liu, Dongsheng Cai. Hypothalamic programming of
systemic ageing involving IKK-β, NF-κB and GnRH. Nature, 2013; DOI:
10.1038/nature12143
*Many of the programs offered by HPC-UK cover this process, especially the specific Anti-Ageing and Brain programs
In the previous article in this series we saw that our evolution as
modern humans was hinged upon a particular adaptation, which was the
development of our extraordinarily large bums. This enabled us (or
rather our ancestors) to become the only species capable of true upright
posture and bi-pedalism which at moderate speeds of locomotion only
cost ¼ of the energy as quadrupedalism.
This adaptation plus a few other benefits of upright posture led us
along the path towards our development of larger brains and with it, the
brains particular requisite needs and amazing abilities. We also saw
that, at the time the most efficient method of providing the nutrient
and energy dense food for our growing brains was through the consumption
of animal tissues which required the use of hunting; particularly the
persistence hunting that requires phenomenal endurance.
However, this is one tiny snippet of our ancestral past that largely
dictates our physiology today. If you read that piece and began to
realise the gulf between many of our lives today and the physical
environmental stress of our forebears, then bear with me as we explore
the rabbit hole a little deeper.
I’m sure you can appreciate
that our evolution occurred over a fairly expansive period of time in
which the environment that our ancestors lived changed considerably,
both from the natural change in the landscape and climatic conditions,
but also due to the migration necessitated for survival. So please
appreciate that there is no single specific activity or type of diet to
which our ancestors would have been exposed; it would’ve been a variable
environment to which our ability to adapt was our saving grace, but
there are some generalisations we can infer from the evidence.
Let’s look at the physical activities in which our ancestors had to
engage to survive. We have already seen that persistence hunting
required travelling distances of up to 20km per day in order to cause
the heat load and exhaustion of the prey which made it easier to kill.
This was mainly performed by males; the females however were not simply
maxing and relaxing back at the shelter waiting for the male to return
with sustenance. They were involved in very vigorous activity, arguably
more vigorous than the males.
From the available evidence it is
proposed that compared to the average distance travelled by males
(15-20km) per day during hunting expeditions, females often covered
45-60% of the distance (9km). As you may have surmised already we still
haven’t introduced the word gathering yet, and this is where the real
action is at. The 9km covered mainly by females was not a contemplative
stroll around the grounds before heading home for tea and scones. It was
an extremely labour intensive essentiality that was a crucial source of
nutrition that buffered the intermittent nature of the more nutrient
dense animal food.
We will visit the food element of this arena
in a later article, but for now we need to appreciate the physical
effort needed to gather sufficient and appropriate non-animal foods was
not akin to a day at a ‘pick your own’.
The principle
non-animal foods were shoots, roots and leaves. The second non-animal
item would’ve been nuts and to a much lesser extent, seeds, with fruit
eaten seasonally. The roots, especially the root tubers, are the most
annually available food as they are protected from the changes in above,
or shallow, ground changes in environment, but this causes a problem
for the gatherer. What problem? They are usually buried 5-6 feet deep in
the ground. I don’t know about you, but in a previous life I worked in
construction and digging holes 5-6 feet deep, even with modern tools, is
tough going. To do this with either your hands or rudimentary tools
would be an imposing task to put it mildly.
And you’d probably
be engaging in the 9km digging-fest filled trek, with a minimum of 7kg
in tow. Why this additional weight? It’s likely that you would be
carrying a baby concomitantly, and also useful materials such as
firewood with which to return to the shelter. While on the subject of
returning with essential items, please bear in mind the males were not
simply going for a walk/ run, wearing down the animal prey and killing
them…job done; they also had to bring the animal back to the shelter and
process the kill, both of which would’ve been fairly monumental tasks.
So both males and females would’ve been engaged in, on a daily basis
some sort of lower (not low) intensity activity for fairly long
durations and also fairly intense activities for slightly less duration,
but still a prolonged period of time. This is in addition, as mentioned
in the previous article, to the acts of shelter creation and
maintenance, tool making, food preparation, climbing and periods of very
high intensity physical activity such as evasion of predators aka
running away…fast.
So, am I saying that we, as modern humans,
need to be covering 9-20km per day, while resistance and/ or gymnastic
training for multiple hours. Not at all. Our ancestors ‘had’ to engage
in this level and type of physical activity for survival. We now have
the ‘luxury’ of not even needing to have to move out of a 10m radius to
exist, should we choose to go that route; our genome, however, doesn’t
thrive in that condition. Our body does require a certain amount of
stress in order to express the genes that create pretty optimal
conditions for a healthy, high performance body and mind. But that
doesn’t mean we have to engage in the exact type and amount of activity,
nor as we shall see the exact food intake, of our ancestors. Both in
physical activity and diet there is scope for a range of nuances,
although there are fundamentals that do need to be acknowledged.
The key point addressed in the previous article, still remains true,
our genome evolved in a very active environment, where nutrition was
hard come by, and it still requires this stimulus today, except we
continue to have to kowtow to our environment, albeit today not so much
dictated by Nature, but certainly culturally. This cultural demand
generally mandates that we are cooped up inside, sat at work stations
for a minimum of 8 hours per day, with an additional 2 hours or so,
spent in similar conditions commuting to and from our places of work.
This leaves 4 hours per day maximum, outside of sleep, in order to do
all of the other activities required in life which includes cooking
meals and supporting our families; especially the very young and old
members. This leaves very little time to fit in the significant amount
of physical activity we have just covered.
So you can’t
realistically replicate your ancestral past exactly, nor would you want
to either. I’ve shown previously that our genome is so amazingly
adaptive that if you begin to ‘up the ante’ for a short period,
especially in the face of food restriction, our genome has no problem in
accounting for this via a metabolic shift; it evolved to deal with this
exact environment. If you set up this situation and then go back to
your old lifestyle then this metabolic shift will bite you in the a*se.
So be careful with the eat less/ exercise more concept, especially if
it’s a self imposed temporary situation of increased activity combined
with nutrient deprivation; you’ll probably end up achieving the opposite
result of the one you nebulously set out to accomplish.
A
better way to go about it is to determine the lowest amount of activity
you can honestly sustain long term and then feed yourself sufficient
high quality food so that you can perform this activity to a high level.
I like this phrase to sum up the idea, and it’s a useful question to
ask yourself daily ‘Have I taken my MED’s* today?’ This seemingly simple
question will, if you do it, literally transform the lives of the
majority of people. Will it create elite performers? Unlikely, that
would take a little more of a precise approach, although surprisingly,
not too much more. But for the greater part of the population a MED
approach would result in a massive improvement in the health,
performance and happiness of the nation. Make sure you get yours.
*Minimum Effective Dose (MED) required to produce a healthy body and mind.
