Hello everyone,

My StandScan Pro arrived today and I'm really impressed! Below my signature 
I've pasted two scans, the first one using the mains adaptor with the StandScan 
Pro, and the second one using the battery. These are double-pages and the two 
are not the same.

Cheers,

Anne

The Art and Science of Low Carbohydrate Living quished (because m p pie then 
returned to a 'balanced,,_ -~ relin.
diet), along with many of its associated metabolic benefits '~ainterla% 
Parallel in time to the popularity of VLCDs, Dr. Robert Atkins promoted a less 
energy-restricted approach to a ketogenic diet. His focus Was on keeping 
carbohydrate intake low enough to induce ketosis, but not to severely limit (or 
even count) calories. To achieve this, he advised individu.
als to eat protein and fat to satiety while keeping dietary carbohydrates low 
enough to maintain positive urine ketones. It was his view that this diet, 
including vegetables, limited fruit, and vitamin supplements, could be followed 
by the individual outpatient without close medical SUpervi.
sion unless there was a pre-existing complicating condition like diabetes or 
hypertension. For most patients, however, the Atkins diet tended to be only a 
temporary sojourn into nutritional ketosis, whether for want of sweets or want 
of approbation from their friends and doctor.
n
,
owever, in these parallel few decades of the VLCD and Atldns diet, hundreds of 
studies were done, and we learned a great deal about carbohydrate restriction. 
Among these lessons are many which can contribute to the safe and sustainable 
use of carbohydrate restricted diets going forward.
Counting Calories vs Carbs It was Dr. Atkins' contention that when most 
carbohydrate was removed from the diet, heavy people lose weight more 
effectively than by classic balanced calorie restriction. The mechanism was 
(and remains) hotly debated. Claims of reduced metabolic efficiency during 
nutritional ketosis remain unproven. Among other points against this is the 
fact that Steve Phinney's bike racers produced the same power output in testing 
0~ a stationary bike using the same oxygen consumption after adapting to the 
Inuit diet compared to their test on a high carb diet[23], leaving little room 
for metabolic inefficiency in this group of subjects.
But this argument over the mechanism of weight loss is an acaderoic straw.man, 
In study after study, over the first 3-6 months, people r~a" 
ClinicaIUse°fCarb°hydrateRestricti°n: VeryL°wCal°rieandLowCarbohydrateDiets 
donaized to a low carb diet eaten to satiety lose more Weight and more body fat 
than those assigned to a low fat, calorie restricted diet. A credible mechanism 
to explain this is not hard to find - carbohydrates in our diet may offer a 
short-term sense of increased energy, but they offer little in the way of 
functional satiety.
~e best example of this effect was reported by Dr. Guenther Boden[45] in an 
inpatient study of obese type-2 diabetics. After a week of eating a balanced 
diet to satiety, the subjects were given a low carbohydrate diet consisting of 
most of the same foods, with the exception that they were asked to limit their 
total daily carbohydrate intake to 20 grams. Over the next two weeks, their 
spontaneous nutrient intakes were carefully measured. Interestingly, the 
subject's average daily energy intake dropped from 3100 to 2100 Calories, and 
this was all due to the 'missing' carbs.
Despite having the choice to eat more, the protein and fat intakes of these 
subjects remained relatively constant. And despite this 1000 Calorie per day 
deficit, their reported hunger, satisfaction, and energy levels did not change 
appreciably. What did change was their diabetes control - dramatically for the 
better. For more on this topic, see Chapter 15.
But this study was just 2 weeks long. What happens in the longer term? Well, 
the process of full metabolic adaptation to a low carbohydrate diet takes up to 
6 weeks, so for the first few months, we would expect wellbeing and function to 
get better. But after many months and a major degree of weight loss, it is a 
normal response of the human body to try to limit its losses. This is typically 
achieved by eating more, but what? If dietary carbohydrate intolerance led to 
the choice of a low carbohydrate diet at the outset, why lift that restriction? 
In particular, why add back calories that promote fat storage but do not 
provide functional satiety? Accepting that protein is good for us only in 
moderation, the answer is fat (see Chapters 2 and 16). How much fat should you 
add as you approach Weight maintenance.~ The simple answer: "let satiety rule", 
163 1~9


-- Made with Prizmo.

Scan 2, using battery

The Art and Science of Low Carbohydrate Living Ketones - To Measure or Not As 
noted m" Chapter 1, nutritional ketosis is defined by ser-um keto ranging from 
0.5 up to 5 mM, depending on the amounts ^€ ~. aes ~'~ uletary car.
boh#rate and protein consumed. In most people, the Combined intake of 100 grams 
of carbohydrate and 100 grams of protein will drive seruna ketones well below 
0.5 mM. While there is nothing magical about hay.
ing circulating ketones above this threshold level, it does have the practi.
cal value of providing the brain with a virtually limitless, fat-derived fuel 
source. This alternative fuel is eminently more sustainable, particularly in 
the insulin resistant or carbohydrate intolerant individual.
Within a few days of starting on carbohydrate restriction, most people begin 
excreting ketones in their urine. This occurs before serum ket0nes have risen 
to their stable adapted level because un-adapted renal tubules actively secrete 
beta-hydroxybutyrate and acetoacetate into the urine.
This is the same pathway that clears other organic acids like uric acid, 
vitamin C, and penicillin from the serum.
Meanwhile, the body is undergoing a complex set of adaptations in ketone 
metabolism[99]. Beta-hydroxybutyrate and acetoacetate are made in the liver in 
about equal proportions, and both are initially promptly oxidized by musde. But 
over a matter of weeks, the muscles stop using these ketones for fuel. Instead, 
muscle cells take up acetoacetate, reduce it to betahydroxybutyrate, and return 
it back into the circulation. Thus after a few weeks, the predominant form in 
the circulation is beta.hydroxybutyrate' which also happens to be the ketone 
preferred by brain cells (as an aside, the strips that test for ketones in the 
urine detect the presence of acetoacetate, not beta-hydroxybutyrate). The 
result of this process of ket0" adaptation is an elegantly choreographed 
shuttle of fuel from fat cells to liver to muscle to brain.
In the kidney, this process ofketo-adaptation is also complex, over ti#, urine 
ketone excretion drops off, perhaps to conserve a valuable enerf/ substrate 
(although urine ketone excretion never amounts to very na#Y wasted calories). 
This decline in urine ketones happens over the s~e 164 
clinicalUseofGarbohydrate Restricti°n: Very L°wCalorieandLowCarbohydrateDiets 
time-course that renal uric acid clearance returns to normal (discussed beloW) 
and thus may represent an adaptation in kidney organic acid metabolism in 
response to sustained carbohydrate restriction.
These temporal changes in how the kidneys handle ketones make urine ketone 
testing a rather uncertain if not undependable way of monitoring dietary 
response/adherence. Testing serum for beta-hydroxybutyrate is much more 
accurate but requires drawing blood, and it is expensive because it is not a 
routine test that doctors normally order.
A non-invasive alternative is to measure breath acetone concentration. Acetone 
is produced by the spontaneous (i.e., non-enzymatic) breakdown of acetoacetate. 
Because it is volatile, acetone comes out in expired air, and its content is 
linearly correlated with blood ketone levels. A number of businesses have 
developed prototype handheld devices to measure breath acetone, but at the time 
of this writing, nothing practical is on the market.
But whatever test is used, the key question is why do it? Many people are able 
to initiate and follow a low carbohydrate diet just fine without ever measuring 
ketones. Others, however, find an objective measure of nutritional ketosis to 
be reassuring. In some clinical settings, ketone testing is used as a measure 
of'diet compliance'. While this may be useful in the short term to keep 
patients on track in a strictly regimented dietary program, it begs the 
question of how that individual's diet will be managed long term. For this 
purpose, the handheld breath acetone monitors under development hold some 
promise as a guidance tool put into the hands of the individual striving to 
find the right levd of carbohydrate intake for long-term maintenance.
Biochemical changes (uric acid, acid/base, dectrolytes, cholesterol 
mobilization)
There are often dramatic but wholly predictable changes that occur in blood 
chemistry values upon initiation of a low carbohydrate diet. As a result, and 
also due to the very limited food intakes of people following very low calorie 
diets, most clinics using them do routine blood tests over the first 165


-- Made with Prizmo.


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