15.5.14

Hyperlipid: Eat as much starch as you wish

Hyperlipid: Eat as much starch as you wish



t
has been interesting to watch the discussions about safe starches on
those rather limited areas of the internet which I frequent. Now, you
have to understand that I have always eaten a certain amount of starch.
Usually chips deep fried in beef dripping to go with a fairly standard
high fat supper. Sweet potatoes and parsnips are the two usual sources.
Certainly two or three times a week. I’m not obese and certainly not
post-obese, so I have some freedom in this. I’ve never been zero carb
though I am very low carb and I run in mild ketosis pretty much all of
the time nowadays.



My routes in to LC, other than the initial window through Atkins, were
Kwasniewski, Bernstein, Groves and Lutz. Lutz was such a nice chap,
certainly in his writing. He was perfectly willing to work at mere LC
levels rather than VLC (72g/d was his advice) and he was very up front
that LC would not work for everyone. For inflammatory bowel disease (he
was a gastroenterologist) he expected progressive improvement over two
years, not two weeks. He discussed that people experiencing failure of
LC for weight loss might eventually need to go to simple calorie
restricted diets (and I guess he knew they would fail on that too). He
had an awareness that exposing an immune system, crippled and
ineffective through years of hyperglycaemia, to sudden onset
normoglycaemia might render if truly functional for the first time in
decades and so exacerbate auto immune attack. Being a medic he would
just reach for a 5 day prednisolone course as a simple expedient. For MS
patients, many of whom respond very well to LC diets, he took them to
around 100g/d initially then down to 72g/d after a few weeks. This is
old stuff.



For people to convert from any particular macronutrient ratio to what is
a modest, rather than very, low carbohydrate diet is fine by me.



What I have found very disturbing is the long list of potentially
catastrophic problems reported to be associated with the type of food
choices I make, where there is an edge of ketosis present much of the
time. I have said before, I like to have a few ketones available.



It is quite possible that I, and virtually every lab rodent ever placed
on a ketogenic diet, might be oddities. Or it might be that 12 years on a
very low carbohydrate diet is too soon for the scurvy, thyroid
deficiency, auto immune attack or glucose deficiency to get me. Perhaps
it will happen tomorrow. But imagine how much money you could save on
genetically the modified mice needed for auto immunity research if a
simple ketogenic diet gave you a virtually free supply.



There is a saying in the medical community (used by those of us with any
sense of self questioning) which goes along the lines of “Clinical
experience is no guide to therapeutic efficacy”. One has only to look at
a cardiologist with a statin prescription in their hand to understand
this. My favourite example is that old chestnut from the siege of Turin
during 1536 when Paré realised that pouring boiling oil in to gunshot
wounds (the Gold Standard medical treatment of the day, to flush out the
toxic carbon particles from the gunpowder residue dontchano) was, to
put it mildly, a bit of a booboo.



So I had a listen to the AHS panel discussion on
safe starches. The first thing I realised was that no one was making a
case for metabolically safe starches, the "safe" referred to a lack of
specific plant poisons. Metabolic safety seemed to be a given. I rather
liked the lady clinician, she sounded just like Lutz. I loved Chris
Kessler too, on C. elegans research. The world is full of people who
seem to think humans are unique, free from the metabolic constraints
which affect mere nematodes. When my own clients query, in wonder, that
cats can get Alzheimers, diabetes, hypertension etc, my reply is that
there is nothing special about humans. Failure to learn from C. elegans
will lead to some interesting booboos, hopefully not as painful as the
boiling oil fiasco.



Ron Rosedale was the only person who came over as making any metabolic
sense or having any deep understanding of the processes involved in the
signalling subsequent to metabolism.



I have an approach to life. I resist insulin. Running on the edge of
ketosis, with a major preponderance of long chain saturated fatty acids
as metabolic substrate, I expect to be insulin resistant. I am. It is
pure physiology. I like to have uncoupled mitochondria running with a
relatively low delta psi, high oxygen consumption and low free radical
leakage. On isolated occasions, a few times a week, my parsnip chips
will spike my blood glucose and delta psi for an hour or so and generate
a few extra superoxide/H2O2 molecules above basal levels. I hope that’s
enough for generating a decent number of healthy mitochondria. I don't
know if I am correct.



So. I think people should feel free to make their own choices about
starch intake. I can't see anything convincing in the concerns that very
low carb eating will run you in to a host of medical problems. I'm very
uncomfortable with the rhetoric. Quote of the year for 2014 comes from
Sid Dishes, relating to the rise of auto immunity caused by VLC eating
(I'm possibly only approximately accurate): "Hypothyroidism is so 2011".
Sid keeps coming up with these lovely phrases on Facebook. Personally I
see no need to add extra starches to what I already eat (between 30 and
60g/d of carbs). This is my rut. I like it.



As we all know only too well, we only get one shot at this. As the Red
Hot Chili Peppers said “This life is more than just a read-through”.



Peter

















14.5.14

Is celiac disease an autoimmune disorder? [Curr Opin Immunol. 2005] - PubMed - NCBI

Is celiac disease an autoimmune disorder? [Curr Opin Immunol. 2005] - PubMed - NCBI



Curr Opin Immunol. 2005 Dec;17(6):595-600. Epub 2005 Oct 7.

Abstract

Celiac
disease, which results from an immune reaction to ingested cereal
gluten proteins, has several autoimmune features. In particular, celiac
disease patients produce highly disease specific IgA and IgG
autoantibodies to tissue transglutaminase when they are on a
gluten-containing diet, and they have small intestinal intraepithelial
lymphocytes which can mediate direct cytotoxicity of enterocytes
expressing MIC molecules in an antigen non-specific manner. Similar to
typical autoimmune disorders, celiac disease has a multifactorial
aetiology with complex genetics, and several autoimmune diseases are
commonly presented by patients with celiac disease. Much has been
learned about the immunology of celiac disease in recent years, and
there is overwhelming evidence that the immune response to gluten is
central to the pathogenesis. In light of this, the many autoimmune
phenomena associated with celiac disease are thought-provoking, and they
challenge us to rethink the boundaries between autoimmunity and
immunopathology.

PMID:
16214317
[PubMed - indexed for MEDLINE]

Publication Types, MeSH Terms, Substances, Grant Support

.....the ability of bacteria to both recognize and synthesize neuroendocrine hormones,The microbial organ in the gut as a driver of... [Med Hypotheses. 2010] - PubMed - NCBI

The microbial organ in the gut as a driver of... [Med Hypotheses. 2010] - PubMed - NCBI



Med Hypotheses. 2010 Apr;74(4):634-8. doi: 10.1016/j.mehy.2009.10.025. Epub 2009 Nov 8.

The microbial organ in the gut as a driver of homeostasis and disease.

Abstract

Based
on the ability of bacteria to both recognize and synthesize
neuroendocrine hormones, it is hypothesized that microbes within the
intestinal tract comprise a community that interfaces with the mammalian
nervous system that innervates the gastrointestinal tract to form a
microbial organ.
Given the evolutionary context in which the central
nervous system is an outgrowth of the more primitive enteric nervous
system and the time in which microbes have colonized the mammalian
intestinal tract, it is further hypothesized that this microbial organ
enters into a symbiotic relationship with its mammalian host to
influence both homeostasis (aspects such as behavior) and susceptibility
to disease. Contained within the overall hypothesis are three main
thematic elements: the species composition of the microbial organ
influences host homeostasis and disease susceptibility; the host's
nervous system influences the species composition of the microbial organ
and the microbial organ itself possesses its own nervous system.
Elucidation of the mechanisms by which this evolutionary symbiosis
occurs would dramatically alter current medical thought by providing a
biological basis for linking these two disparate organ systems and
provide a new paradigm with which to understand and design new
therapeutic approaches for a range of clinical diseases.

(c) 2009 Elsevier Ltd. All rights reserved.
PMID:
19900764
[PubMed - indexed for MEDLINE]

Are bacteria making you hungry? -- ScienceDaily

Are bacteria making you hungry? -- ScienceDaily



American Society for Microbiology


Summary:


Over
the last half decade, it has become increasingly clear that the normal
gastrointestinal (GI) bacteria play a variety of very important roles in
the biology of human and animals. Now researchers propose yet another
role for GI bacteria: that they exert some control over their hosts'
appetites.





Are
bacteria making you hungry? Over the last half decade, it has become
increasingly clear that the normal gastrointestinal (GI) bacteria play a
variety of very important roles in the biology of human and animals.


Over
the last half decade, it has become increasingly clear that the normal
gastrointestinal (GI) bacteria play a variety of very important roles in
the biology of human and animals. Now Vic Norris of the University of
Rouen, France, and coauthors propose yet another role for GI bacteria:
that they exert some control over their hosts' appetites. Their review
was published online ahead of print in the Journal of Bacteriology.




This
hypothesis is based in large part on observations of the number of
roles bacteria are already known to play in host biology, as well as
their relationship to the host system. "Bacteria both recognize and
synthesize neuroendocrine hormones," Norris et al. write. "This has led
to the hypothesis that microbes within the gut comprise a community that
forms a microbial organ interfacing with the mammalian nervous system
that innervates the gastrointestinal tract." (That nervous system
innervating the GI tract is called the "enteric nervous system." It
contains roughly half a billion neurons, compared with 85 billion
neurons in the central nervous system.)


"The gut microbiota
respond both to both the nutrients consumed by their hosts and to the
state of their hosts as signaled by various hormones," write Norris et
al. That communication presumably goes both ways: they also generate
compounds that are used for signaling within the human system,
"including neurotransmitters such as GABA, amino acids such as tyrosine
and tryptophan -- which can be converted into the mood-determining
molecules, dopamine and serotonin" -- and much else, says Norris.


Furthermore,
it is becoming increasingly clear that gut bacteria may play a role in
diseases such as cancer, metabolic syndrome, and thyroid disease,
through their influence on host signaling pathways. They may even
influence mood disorders, according to recent, pioneering studies, via
actions on dopamine and peptides involved in appetite. The gut
bacterium, Campylobacter jejuni, has been implicated in the induction of anxiety in mice, says Norris.


But
do the gut flora in fact use their abilities to influence choice of
food? The investigators propose a variety of experiments that could help
answer this question, including epidemiological studies, and
"experiments correlating the presence of particular bacterial
metabolites with images of the activity of regions of the brain
associated with appetite and pleasure."

Story Source:

The above story is based on materials provided by American Society for Microbiology. Note: Materials may be edited for content and length.

Journal Reference:

  1. V. Norris, F. Molina, A. T. Gewirtz. Hypothesis: bacteria control host appetites. Journal of Bacteriology, 2012; DOI: 10.1128/JB.01384-12

Cite This Page:

American
Society for Microbiology. "Are bacteria making you hungry?."
ScienceDaily. ScienceDaily, 19 December 2012.
<www.sciencedaily.com/releases/2012/12/121219142301.htm>.

4.5.14

Substituting monounsaturated fat with saturated = more active and better mood ... [Am J Clin Nutr. 2013] - PubMed - NCBI

Substituting dietary monounsaturated fat for ... [Am J Clin Nutr. 2013] - PubMed - NCBI



Am J Clin Nutr. 2013 Apr;97(4):689-97. doi: 10.3945/ajcn.112.051730. Epub 2013 Feb 27.

Substituting
dietary monounsaturated fat for saturated fat is associated with
increased daily physical activity and resting energy expenditure and
with changes in mood.

Erratum in

  • Am J Clin Nutr. 2013 Aug;98(2):511.

Abstract

BACKGROUND:

The Western diet increases risk of metabolic disease.

OBJECTIVE:

We
determined whether lowering the ratio of saturated fatty acids to
monounsaturated fatty acids in the Western diet would affect physical
activity and energy expenditure.

DESIGN:

With the use of a
balanced design, 2 cohorts of 18 and 14 young adults were enrolled in
separate randomized, double-masked, crossover trials that compared a
3-wk high-palmitic acid diet (HPA; similar to the Western diet fat
composition) to a low-palmitic acid and high-oleic acid diet (HOA;
similar to the Mediterranean diet fat composition). All foods were
provided by the investigators, and the palmitic acid (PA):oleic acid
(OA) ratio was manipulated by adding different oil blends to the same
foods. In both cohorts, we assessed physical activity (monitored
continuously by using accelerometry) and resting energy expenditure
(REE). To gain insight into a possible mood disturbance that might
explain changes in physical activity, the Profile of Mood States (POMS)
was administered in cohort 2.

RESULTS:

Physical activity
was higher during the HOA than during the HPA in 15 of 17 subjects in
cohort 1 (P = 0.008) (mean: 12% higher; P = 0.003) and in 12 of 12
subjects in the second, confirmatory cohort (P = 0.005) (mean: 15%
higher; P = 0.003). When the HOA was compared with the HPA, REE measured
during the fed state was 3% higher for cohort 1 (P < 0.01), and REE
was 4.5% higher in the fasted state for cohort 2 (P = 0.04). POMS
testing showed that the anger-hostility score was significantly higher
during the HPA (P = 0.007).

CONCLUSIONS:

The replacement
of dietary PA with OA was associated with increased physical activity
and REE and less anger. Besides presumed effects on mitochondrial
function (increased REE), the dietary PA:OA ratio appears to affect
behavior. The second cohort was derived from a study that was registered
at clinicaltrials.gov as R01DK082803.

PMID:
23446891
[PubMed - indexed for MEDLINE]

PMCID:
PMC3607650

Free PMC Article

3.5.14

Against Autophagy - Diet Dogma Rears Ugly Head Again: Become a Fat Burner, Eat Your Own Crap, and Live Longer

Andrew Kim Blog: Diet Dogma Rears Ugly Head Again: Become a Fat Burner, Eat Your Own Crap, and Live Longer



Whether we like it or not,
autophagy will occur in all of our cells. 
It is a primitive form of protection that allows cells to dispose of misfolded
proteins, misassembled protein complexes, damaged mitochondria, and so
forth.  There is absolutely no need or
reason to force it to occur artificially with special diets – especially so if
you’re already healthy.  Undue misery is sure to follow from this
self-imposed deprivation.  Interestingly,
all the conditions that bring about autophagy are at odds with the conditions
that maximize our potential as organisms, and this entails the thyroid hormone
and oxidation of glucose for fuel.  I
think it’s time for us to toss the idea of diet-induced autophagy into
the pile
with the other worthless dogmas that have done little more than leave
the landscape of diet and nutrition understanding in disarray.  

1.5.14

Diet Dogma Rears Ugly Head Again: Become a Fat Burner, Eat Your Own Crap, and Live Longer - Andrew Kim Blog

Andrew Kim Blog: Diet Dogma Rears Ugly Head Again: Become a Fat Burner, Eat Your Own Crap, and Live Longer



Holding my dog up against my
chest moments before he had peacefully taken his last few breaths this past
Saturday evening, I thought about how cold his hands and feet were; how
slow his heart beat and breathing were; and just how much he had shrunk and atrophied.  Of course, these are all
the consequences of aging, a topic that I try to avoid thinking about as all
get out because thinking about aging inevitably leads to an inner dialogue
about your own mortality, or the mortality of those close to you. 

Lo and behold, there is a
great amount of money spent on all the things that could potentially delay the
aging process and the advent of the diseases associated with it – including,
but by far not limited to, hormone replacement therapy and massive vitamin
supplementation.  Unfortunately, this
desire to push back Father Time has spawned and perpetuated some pretty awful
ideas which have no basis in any reasonable level of evidence. 


One such idea, actually a
few related ideas that I’ll roll into one idea here, is to limit the amount of
glucose our cells burn over the course of a lifetime, so as to turn on a primitive
stress response mechanism called autophagy, a process whereby cells degrade and
recycle their dysfunctional components in the face of nutrient depleted
conditions.
  Unfortunately, this
necessarily entails burning proportionately more fatty acids for fuel (or
what’s called being “fat adapted” in horribly egregious articles filled
with wishful thinking like this
one) and turning
down thyroid functioning, or the rate at which we live, adaptations that are directly
at odds with reaching our full potential as human beings.



Mainly, the physiological changes
which I am most interested in are the increased secretion of ACTH, insulin, and beta-endorphins
(anandamides
and
2-araichdonylglycerol [derived from arachidonic acid])
and decreased
secretion and tissue responsiveness to the thyroid
hormones
– all of which are disease-promoting in excess, while incidentally
predisposing to weight gain.  ACTH is a
subject that deserves its own post. 
Ditto for the beta-endorphins. 
The discussion herein will center on the thyroid hormone, especially
since I’m highly motivated at this moment to avoid all quibbling over insignificant
details and minutiae at all costs.

Maintaining tissue
responsiveness to hormones is, I believe, a key factor in slowing down the
aging process.  Consider Progeria, a syndrome famous for
producing an apparent accelerated aging in children.  Progeria is characterized by a massive
reduction in the responsiveness of cells to all hormones – a defect
thought to drive the degenerative conditions that appear in
children with the condition.

 
A cell’s responsiveness to
hormones is most sensitive when the stress hormones, free amino acids, and free
fatty acids in the blood are low. For example, a deficiency of growth hormone,
a stress hormone secreted by the pituitary gland, leads to an inflated
sensitivity to the hormone insulin in adulthood.1

Next, consider for a moment people
who diet often.  Despite having normal lab tests these people
will experience all the signs and symptoms of hypothyroidism.  This paradox indicates a reduced sensitivity
of tissues to the thyroid hormones, brought about by the stress of
under-eating.  In point of fact, the
uptake of thyroid hormones into the central nervous system is impaired by high
levels of the stress hormones, free amino acids, and free fatty acids.2 In the central nervous system, the thyroid hormones,
in conjunction with the sex hormones, are not only essential for brain
development, but also for brain growth, repair, and maintenance in adulthood.3

A low carbohydrate diet,
another self-imposed stressor, not only impairs the ability of cells to uptake
thyroid hormone, but also hampers the conversion of T4 (pro-hormone)
to T3 (active hormone) in the body or directs the conversion of T4
to reverse T3 (inactive hormone), rather than T3.  These conversion problems could alternatively
explain the pattern of having normal lab tests and hypothyroid signs and
symptoms.4 In the pituitary gland, for example, anything that
inhibits the production of 
T3 from T4 disinhibits the
release of TSH, resulting in the following pattern:
TSH, T4, and T3.5

The thyroid hormones are the
principle regulators of all the things concerned with metabolism, including the
process of tissue repair and renewal.  Because
the thyroid hormone both facilitates the release of glucose from the liver and
stimulates the uptake and oxidation of glucose in the tissues outside the liver
(thereby working antagonistically and synergistically with insulin,
respectively) there’s really no surprise here.6 In fact, even topically applied active thyroid
hormone accelerates wound healing and repair following injury.7

But in so turning up the
metabolism by way of the thyroid and supplying nutrient replete conditions to
cells, are we not incidentally shutting off the mysterious and magical powers
of autophagy?

Another feature of Progeria,
which animal models of Progeria and the like have unexpectedly found, is an increase in autophagy – an effect touted
as highly desirable among Paleo, low-carbohydrate, and caloric restriction
advocates.  The molecular mechanisms are
not well understood, but it does help to explain, to me at least, why chronic
dieters look so haggard and the opposite of healthy, vibrant, and attractive;
sometimes, as if death has warmed over.  Simply put, autophagy is an adaptive
response to metabolic stress that when chronically activated drives premature
aging by inducing catabolic processes that outpace the renewal ability of
cells
.8 An increased oxidization of fat in preference to
glucose is a key feature underlying this downward metabolic shift, as well as
an impairment of mitochondrial respiration and a decline in ATP levels. 

As an aside, the fact that
Internet diet gurus had made a claim – which probably led to undue misery –
about their diets based on a study in a roundworm should piss you off.

The positive
association between resting metabolic rate and maximum lifespan may suggest two
things.  The first is that without having
to call upon the mysterious and magical powers of autophagy, a high resting
metabolic rate accelerates cell protection and repair mechanisms by way of
enhanced protein synthesis.  The second
is that the thyroid hormones are efficiently acting on their target tissues on
which they activate the uncoupling proteins, thereby diffusing the reductive
stress imposed on cells (by for instance a sluggish metabolism) to discourage
the formation of reactive oxygen species and oxidative stress.

Patented, synthetic thyroid hormone
products are on their way to the market pending approval by the FDA and, from
the outside looking in, they seem to be highly effective for all the conditions
for which a deficiency of thyroid hormone directly cause, from easy fat gain to
heart disease.  They also would eradicate
the uncertainties associated with glandular products and the cardiovascular
side effects associated with the synthetic products because thyroid hormones,
to be effective, only really require
identical big and bulky groups attached to each of their two tyrosine
amino acid residues to restrict movement around the bond which holds these two tyrosine
amino acid residues together via an ether linkage. (I wanted to blog about this
in the past but I was 99.97% sure it would interest no one.) 

Whether we like it or not,
autophagy will occur in all of our cells. 
It is a primitive form of protection that allows cells to dispose of misfolded
proteins, misassembled protein complexes, damaged mitochondria, and so
forth.  There is absolutely no need or
reason to force it to occur artificially with special diets – especially so if
you’re already healthy.  Undue misery is sure to follow from this
self-imposed deprivation.  Interestingly,
all the conditions that bring about autophagy are at odds with the conditions
that maximize our potential as organisms, and this entails the thyroid hormone
and oxidation of glucose for fuel.  I
think it’s time for us to toss the idea of diet-induced autophagy into
the pile
with the other worthless dogmas that have done little more than leave
the landscape of diet and nutrition understanding in disarray. 


REFERENCES

1.       Bartke, A., Sun, L. Y. & Longo, V.
Somatotropic signaling: trade-offs between growth, reproductive development,
and longevity. Physiol. Rev. 93, 571–98 (2013).
2.       Hennemann,
G. et al. Plasma membrane transport of thyroid hormones and its role in
thyroid hormone metabolism and bioavailability. Endocr. Rev. 22,
451–76 (2001).
3.       Correia,
H. R., Balseiro, S. C. & de Areia, M. L. Are genes of human intelligence
related to the metabolism of thyroid and steroids hormones? - endocrine changes
may explain human evolution and higher intelligence. Med. Hypotheses 65,
1016–23 (2005).
4.       Araujo,
R. L. et al. High-fat diet increases thyrotropin and oxygen consumption
without altering circulating 3,5,3’-triiodothyronine (T3) and thyroxine in
rats: the role of iodothyronine deiodinases, reverse T3 production, and
whole-body fat oxidation. Endocrinology 151, 3460–9 (2010).
5.       Larsen,
P. R., Dick, T. E., Markovitz, B. P., Kaplan, M. M. & Gard, T. G.
Inhibition of intrapituitary thyroxine to 3.5.3’-triiodothyronine conversion
prevents the acute suppression of thyrotropin release by thyroxine in
hypothyroid rats. J. Clin. Invest. 64, 117–28 (1979).
6.       Brenta,
G. Why can insulin resistance be a natural consequence of thyroid dysfunction? J.
Thyroid Res.
2011, 152850 (2011).
7.       Safer,
J. D., Crawford, T. M. & Holick, M. F. Topical thyroid hormone accelerates
wound healing in mice. Endocrinology 146, 4425–30 (2005).
8.       Mariño,
G. et al. Premature aging in mice activates a systemic metabolic
response involving autophagy induction. Hum. Mol. Genet. 17,
2196–211 (2008).


Angry fat: the new lifestyle hazard to watch

Angry fat: the new lifestyle hazard to watch



Angry fat: turn down the heat.
Angry fat: turn down the heat. Photo: Mustafa Arican
It is estimated that as much as 70 per cent of cancer is lifestyle-related.

There are also established links between being overweight and the risk of cancer and other chronic diseases.

But, it is not just fat that is the problem. Rather, what Dr Lise Alschuler refers to as "angry fat" may be to blame.

"The data shows pretty clearly that obesity in the US is
responsible for one in every six deaths and one in every five
diagnoses," says Alschuler, founding board member of the Oncology
Association of Naturopathic Physicians and co-author of The Definitive Guide to Cancer: An Integrative Approach to Prevention, Treatment and Healing.

"What we're now learning is the mechanism between extra weight and cancer. I phrase it as 'angry fat'."

When there is excess glucose circulating in the blood,
triglicerides, which are a type of fat, store in the fat cells, she
explains.

When this happens the fat cells start to swell and send "distress" signals.

This 'distress' or inflammation, "triggers the production of a
range of chemicals and hormones that can turn on inflammation and
damage cells directly and stimulate uncontrolled cell growth
systemically," Alschuler, herself a breast cancer survivor, says.

This means that health is not just about losing fat but looking to make fat less "angry".

"There are overweight people who aren't insulin-resistant or have angry fat," explains Alschuler.

She notes that insulin resistance and being overweight are not always the result of diet and "it's not just about sugar".

That said, addressing diet and other lifestyle factors can certainly help to calm cranky cells.

To turn down the internal heat and minimise our risk of
inflammation and insulin-resistance, Alschuler, who was recently in
Sydney to speak at the BioCeuticals Symposium, suggests:

1. Calorific restriction. "Most of us consume too much."

2. Manage glycaemic load. "Foods that reduce the glucose load in the body include cinnamon, blueberries and spices," she says.

"Low GI is also consistent with Mediterranean and Paleo diets
which advocate minimal consumption of refined, processed carbohydrates.
They are also anti-inflammatory."

Although the Paleo diet tends to be heavy in animal protein,
which has been linked to cancer, Alschuler points out that the type of
meat consumed makes a difference.

The Paleo diet advocates eating pasture-fed meat, which has been found to have less fat as well as more omega-3 fatty acids.

Still, when it comes to meat, considering quantity is as
important as quality. "One of the triggers is excessive saturated fat -
particularly animal fat," says Alsculer. "It's worth considering."

3. Eat a rainbow on a plate (made up of
natural, not synthetic colours). Polyphenols are a type of antioxidant
which have very potent anti-inflammatory effects. There are more than
4000 types of polyphenols found in different fruits and veggies, so
variety is key. "They are also anti-insulin resistant and directly
anti-cancer," Alschuler says.

4. Support the body with good fats, like omega-3s and other health-supporting nutrients.

"Co-q 10, which is found in food and supplements and supports the pancreas, liver and kidneys," Alschuler says.

5. Make a good night's sleep a priority. "One night of sleep-deprivation will cause someone to be insulin-resistant the next day."

6. It's not about juice-fasts or quick
fixes. "Persistent organic pollutants are irritating to fat cells, but
the answer would be less 'detoxify' on a three-day juice fast," she
says. "For this purpose, it's really a long-term commitment to how we
support our natural detoxification process ...

"It's typically a gentle daily process - optimising intestinal function and adding a lot of antioxidants to the diet."

7. We don't have to ditch our favourite
foods or drinks. "I'm a big fan of organically grown coffee. It's a rich
source of polyphenolic compounds and green tea," Alschuler says.
"[Similarly] I'm not averse to grains if they're whole and organic. But
the more processed they are, the more likely they are to be converted to
glucose."

8. Sometimes it's nothing to do with food
and everything to do with attitude. "It's not about reproachfulness -
that will only aggravate the whole thing," she says. "Any health
improvement has to be couched in self-love and respect. Not only to make
it sustainable but to make it successful.

"Chronic stress feeds the cycle of chronic inflammation and elevates blood sugars."