Personal experience with LCHF since 2011

I have tried to be consistent with Low carbohydrate High Fat diet or Atkins type diet for 8 years.  Most of the time I was in nutritional ketosis documented at 0.5 or greater by serum checks. 

I have read Eat Rich Live Long published in Feb 2018.  
I agree that early diagnosis of insulin resistance needs to be made with 2 hour post prandial glucose and insulin level.  I think this might make major inroads in preventing the next obesity pandemic by getting people on LCHF diet early in their life. 

However I have two major problems with the advice of Eat Rich Live Long on:
1- How to Maintain Weight loss 
2-How to treat high CAC score and high LDLc or LDLp or ApoB or non-HDL cholesterol. 

See my review of Eat Rich Live Long link. 

Despite being on LCHF my HgbA1c remains at 7.7.  Losing 75 lbs in 2006 did not cure my DM2 problem.  What has kept me from progressive cardiovascular disease is my great lipid reductions from: 
Atorvastatin (lipitor) 10 mg 
Endur-acin (over-the-counter Niacin) 1,000 mg. 

My  results from inexpensive standard lipid panel 4-3-18
FASTING
Total Cholesterol 144
HDLc                     58
nonHDLc               78   (most important risk parameter on standard lipid panel)
LDLc                      66  (standard for trials but not accurate w high TG  discordance)
Triglycerides          64
Remnants               13 (greater than 35 is risk factor )
Hgb A1c                 7.7 (not on insulin, on metformin, invokana and victoza)
Bioelectrical 4 point Impedance Scale
Wt. 206.8 pounds, 
Body Fat 25.6%, 
Fat Free mass 74.5% 
Body H2O 55.5%
Muscle Mass 38.8 pounds
BMI 28.6
Waist 41.5 inches
Visceral fat 15


Liposcience Advanced Lipid testing 3-23-18
Non-fasting
Total Cholesterol 144
HDLc                     60
non-HDLc              84  (goal less than 80)
LDLc                      66
Triglycerides          92 
Remnants               18   (TC minus HDLc minus LDLc) 
HDLp                     39.4  (problem with TC/HDLc ratios is no discernment between large/small HDLp)
small LDLp          312 (normal)(<750 b="" this="">not important if LDLp less than 750)
LDLp                    661  <750 font="" nbsp="">(the best predictor CVD)
LDL size              20.2 (normal)

VLDLp                    4.5 (high) (non-fasting)
VLDL size             51 (high)  (non-fasting)
LP-IR score            45 (normal) (not sure what to make of this I have DM2)        

Fasting AM serum ketones:
3/29     0.3
3-30     1.6
3-31     0.7
4-1       0.8
4-2       0.6 


Up to Date take away message.
1-The most important inexpensive risk factor is non-HDL cholesterol.

2- The best and most accurate risk factor is with advanced testing for particles.
Either LDLp or ApoB

3- Getting triglycerides down with LCHF, Lovaza (fish oil) and niacin is very important as well, especially for insulin resistant patients. 

4- LCHF diet and nutritional ketosis will not be sufficient treatment in many cases, especially if CAC is greater than 100.
Statins, Zetia and Endur-acin (niacin) in low doses together can get particles down very low and even reverse plaque.   Low doses have less side effects. 

5- To reverse plaque on CAC or CIMT get:
non-HDL cholesterol less than 80 or
LDLp less than 750 or 
ApoB less than 80
and 
Triglycerides less than 100


To see several years of my CAC scores and CIMT with evidence of reversal of plaque go to my CAC and CIMT scores link

link to my Review of Eat Rich Live Long 

I agree with #LCHF diet especially as concerns Insulin Resistant or DM2 patients.

I don't agree with their approach to treatment of high CAC or high LDLc (cholesterol), Non-HDLc, ApoB or LDLp (particles)

Adding phentermine to Belviq

Off-label drugs for weight management.

Nice article from 2017 on diet medications posted below. 

Belviq (Locaserin) is a good first choice in choosing a diet medication.  

It has few side effects but trials show only 50% efficacy.

Hence, a physician should add generic low dose phentermine after two months on Belviq. 

This is very similar to the old combination of  fenfluramine/phentermine (Podimin) which was taken off the market for possible heart valve problems and deaths from pulmonary hypertension. 

Belviq is similar to fenfluramine but has specific receptors that don't affect the heart valves. 

The physician must have a DEA number(drug enforcement agency) to prescribe these scheduled IV drugs. 

Your physician may ask you to sign an agreement for the off-label use of phentermine.  

Diabetes Metab Syndr Obes. 2017 Jun 10;10:223-234. doi: 10.2147/DMSO.S95299. eCollection 2017.

Hendricks EJ1.

Author information

Abstract

The global pandemic of obesity and overweight now affects between 2.8 and 3.5 billion of the world population and shows no signs of abatement. Treatment for what is now recognized as a chronic disease includes pharmacotherapy, considered an essential component of comprehensive therapy. New drug discovery is robust, but the pace of the US Food and Drug Administration approval for obesity drugs has been glacial, and only a handful of approved drugs are available for treating obesity. In the last 20 years, the US Food and Drug Administration has approved 208 drugs for cancer, 118 for cardiovascular diseases, 168 for neurological diseases, and 223 endocrinologic drugs, but only 6 for obesity, 2 of which have been taken off market. Currently, there are only 9 drugs approved by the FDA for obesity treatment. US physicians have turned to off-label drug use in their effort to care for increasing numbers of patients with excess adiposity. Phentermine is the most commonly used drug for treating obesity. Although approved only for short-term use, US physicians have used it successfully for long-term since its initial approval in 1959. This drug, used off-label for long-term, has proven to be safe and effective, far safer than the disease it is used to treat. Phentermine and diethylpropion, an equally safe but somewhat less effective drug, are both generic and therefore inexpensive. These drugs have been maligned inappropriately because their two-dimensional structure diagrams resemble amphetamine and also because of unproven presumptions about their potential adverse effects. In the face of an increasing epidemic, worldwide obese and overweight patients deserve effective treatment that prescribing these drugs could provide, if rehabilitated and used more frequently. US physicians will likely continue to use any drug proven useful off-label for this illness until such time as more effective drugs are approved.

This is a slide from Medscape link

To read about the waterfall results of Bariatric Surgery, LOOK AHEAD trial, and a one minute video on ATOZ trial click my blog

I believe I have maintained my 80 pound weight loss over 11 years by using multiple diet medications and the lessons I have learned can be applied to others with Chronic Obesity.

My findings are available for $3.03 on Amazon kindle at
 The Chronic Disease of Obesity/How Sponge syndrome causes weight regain

The Science of Nutritional ketosis in LCHF diet

Easier reading of the excerpts at my google document. 


To go to the original article see:

Front Psychol. 2015; 6: 27.

Published online 2015 Feb 2. doi:  10.3389/fpsyg.2015.00027

Excerpt One 

"There are two distinguished types of food intake regulation:

a) the short-term (satiety signals, SS) occurring at the beginning and end of a single meal;
it also includes the length between meals and

b) the long-term regulation (adiposity signal, AS) that is influenced by such factors
as body fat deposition."

Excerpt two

"Hormones like leptin and insulin, both secreted into the blood,
reflect the stored body fat.
These hormones can pass the BBB and stimulate specific receptors.
Hypothalamic areas are richly supplied by axons from ARC,
which has greater concentrations
of leptin and insulin receptors than any other hypothalamic site (Valassi et al., 2008).

The ARC exerts opposing actions on food intake responding not only to leptin and insulin,
but also to gut hormones (the most studied are ghrelin and, recently, PYY).
The neurophysiological pathways suggest that feeding is regulated by a feedback loop,
where the hypothalamus provides the long-term regulatory input to the NTS,
which acts as a setpoint (Williams et al., 2001).

It has recently been proposed that the ARC is required for the
coordination of homeostatic circadian systems including temperature and activity."

Excerpt three

Many molecules produced by the GIT exert hunger or satiety effects on the brain."

Ghrelin

Cholecystokinin (CCK) Three other related hormones are

1- pancreatic polypeptide (PP),

2- amylin, and

3- peptide YY (PYY).

Amylin Peptide YY (PYY)

glucagon-like peptide 1 (GLP-1)

"The gut-brain link is important not only for the hormones produced by the gut,
but also for the long-term body weight regulation."

Excerpt four


"It is important to note that during physiological ketosis (fast or very low calorie ketogenic diets)
ketonemia reaches maximum levels of 7–8 mmol/L
with no change in blood pH,
while in uncontrolled diabetic ketoacidosis blood concentration of KBs can exceed 20 mmol/L
with a consequent lowering of blood pH
(Robinson and Williamson, 1980; Cahill, 2006) (Table ​(Table11).

We can say that no species, including humans,

could have survived for millions of years without the ability to withstand
brief periods of hunger or starvation (Amen-Ra, 2006).

These periods of fasting are themselves ketogenic (McCue, 2010)
during which the concentrations of insulin and glucose decrease

while that of glucagon increases in the attempt to maintain normal blood glucose levels.

When the body passes from a condition of food abundance to one of deprivation
(or else via VLCKD simulated deprivation), there is, with a slight delay,
an increase in the concentration of free FAs as well as KB in the blood.

Thus,
from this point of view KD could be compared to caloric restriction for fasting. "

Excerpt five

Effects of ketosis on hunger and satiety

"Although convincing, the bulk of evidence
in relation to the inhibitory effects of ketosis on appetite is still anecdotal.

Preliminary scientific reports seem to support this phenomenon,
and the evidence shows that KD is more effective,
at least in the short/medium-term, on fat loss (Paoli, 2014).

It was demonstrated that diet-induced weight loss
leads to changes in energy expenditure and in appetite-regulating hormones
that facilitate weight regain and the return to initial energy homeostasis
(Sumithran et al., 2011).

This response to alteration of energy balance
nullifies the success of many dietary approaches.

It is well-known that the long-term success of a nutritional approach is defined
by the amount of weight regain and is the main problem
regarding the so-called weight cycling or “yo-yo” effect (Jeffery, 1996).

A recent study by our group has demonstrated that a brief ketogenic period,
if followed by a longer period of correct Mediterranean diet
could avoid this yo-yo effect (Paoli et al., 2013)."

INSERT:Brian Edwards note: this long term study was only 12 months long.

Excerpt six

"Recently, Sumithran et al. demonstrated that there is a long-term persistence of changes
in some peripheral hormones involved in food control (Sumithran et al., 2011).
In this study,
they found a significant difference in mean levels of many food intake-related hormones
1 year after the cessation of weight loss via the hypocaloric diet.
There was a long lasting decrease of anorexigenic compounds:
1-leptin,
2-PYY,
3-cholecystokinin,
4- insulin, and
5- pancreatic peptide and an
6-increase of the orexigenic molecule ghrelin.
Moreover,
they found that hunger remained elevated 1 year after diet cessation.
In a successive study the same group investigated hunger-related hormones
after 8 weeks of KD, demonstrating that during ketosis the increase of ghrelin
(a strong stimulator of appetite) was suppressed (Sumithran et al., 2013).
These results are consistent with those of Ratliff et al (Ratliff et al., 2009),
who found no significant change in fasting plasma ghrelin after 12 weeks of VLCD."

Excerpt seven

"The global picture is complicated by the contradictory role of ketosis on
anorexigenic and orexigenic signals (summarized in Figure ​Figure4).4).

Ketones (mainly BHB) can act both orexigenically or anorexigenically."

INSERT my comment: Insulin acts peripherally anabolic, and centrally catabolic.
Leptin and Insulin act on the same pathways centrally. (i.e on inhibiting Ghrelin)

Excerpt of Epilogue from Chronic Disease of Obesity

This is an excerpt from The Chronic Disease of Obesity

Easier reading can be found on my google document

Epilogue

The main message of this book is that The Sponge Syndrome will cause
weight regain despite Atkins diet and exercise because
the low leptin levels tell your brain you are starving.
Subsequently multiple compensatory hormonal pathways are utilized
to make a reduced obese patient re-gain weight
even at relatively low calorie intakes.

I believe by my personal experience of having Chronic Obesity,
the only way to maintain weight loss for greater than 10 years with satiety is 
with the addition of multiple diet medications.  

Satiety on a restricted caloric diet is crucial to maintain that diet
for the long term.

Major challenges to treatment of chronic obesity:

1- Diet Medication high cost

2- Must stay on diet medication for rest of life.

3- Must stay on restrictive diet for rest of life.

People are offered bariatric surgery rather than trying a LCHF diet
with nutritional ketosis.  

Physicians must learn about diet medications and use them as a first drug.
If on Insulin with Diabetes Type 2 for example switch to
Metformin, Victoza or Invokana.

Don’t ever tell a reduced obese patient,
they regained weight because they didn’t exercise enough
(60 to 90 minutes/day) or stick to a starvation diet (1500 cal/day).
This may be in the guidelines but
it did not work over 10 years in the LOOK AHEAD trial
despite the best institutional support in the treatment group.

Ask your Doctor if he had read Gina Kolata NYT article on
The Biggest Loser.  
They regained even though they did everything right.

It is all about never losing your fat cells.  When adipocytes

are shrunken in the reduced obese,
they are low in Leptin and tell your brain you are starving.
MiRNA from the numerous fat cells then send same message
(starvation) to most of the body
in the form of episomes in the blood stream.  

Remember 70% of your resting metabolism is from the
liver, brain and kidney.
When these organs are tuned down in metabolism
no amount of exercise can overcome it.
More exercise makes a patient more hungry.

The only way to fight the Sponge Syndrome is with
multiple diet medications.

Finally, find a physician certified in the American Board of Obesity Medicine
who has a good bioelectric impedance weight scale so you can follow your muscle mass.
 It will be discouraging to see the 5-10% loss of muscle mass
as you lose weight.

First Body Composition Report before starting Qysmia 
at Stormont Obesity Clinic
6-23-15 244.8 lbs 46.1 lbs muscle mass

12-11-15 222.1 lbs 41.8 lbs muscle mass

4-11-18  204.3 lbs Muscle Mass 38.4 lbs.

5-11-18 vs 5-3-18 at 210 lbs after wt lifting

I think it is more important to lose as much weight as possible in the first 6 to 9 month window.  Then at the plateau, start the low weight high repetition (24 reps, 3 sets, 4 times a week) exercises on very high protein diet (2.4 mg/d protein per kg of lean body weight).

With more exercise is more hunger.  This is why you will need the diet medications more than ever.