Rather than picking an arbitrary number for vanity there’s a better way. BMI may be the worse way possible (this Smart BMI page does better). Looking at pictures of other people is probably the second worse possible way. To pick your goal weight you should take these things into account –
- Lean Body Mass
- Ideal Body Fat
Each of these can be determined fairly easily.
I’m going to assume that you know your gender although that may not be a safe assumption.
Determining your Lean Body Mass
There are on-line calculators which let you determine your Lean Body mass. Here’s one of them (US Navy Calculator – Body Fat Calculator). For an example, I put in my current numbers:
That has my Lean Body Mass at 142 lbs and my current Body Fat percentage at 21%.
Ideal Body Fat Percentage by Age
The ideal body fat percentage can be found in various on-line charts such as (Ideal Body Fat Percentage by age) –
I am 55 years old and they have my idea body fat percentage at 20.9%. Pick your own number from above.
The goal weight is the Lean Body Mass divided by (1 minus the ideal body fat percentage). For me that’s –
142 (Lean Mass from the US Navy calculator above) divided by (1 minus .209 from the Ideal Body Fat percentage chart at my age) = 179.5 lbs
I am at 180.4 so I am within 1 lb of my ideal weight.
What about people who say that they are not losing weight but they are losing inches? The comment is often something like this:
with the increased protein intake of the keto diet, our bodies produce more muscle mass instead of fat deposits like on a carbohydrate rich diet. Muscle weighs more than fat so that would explain fat disappearing but scale numbers not changing
Maybe… Or maybe not…
Muscle is more dense (lower volume) per pound than fat (article). But gaining muscle mass is very slow. Lyle McDonald say that a young untrained male who begins training can put on as much as two lbs of muscle mass in a month. A woman can put on around half that much. So the rate that people are actually putting on muscle mass is pretty small. And unless someone is exercising pretty hard they won’t put on nearly as much. And older people will put on muscle even slower.
So the if someone is stalled for a couple of days or even weeks it’s not likely that they have put on much muscle mass in that time period. Given months, maybe they have put on some.
But this point can be answered by measuring a person’s body fat percentage.
So, there could be some muscle replacement. Or there could be loss of lean body mass. How do you tell the difference? Take measurements with a tape measure and use a calculator to determine your muscle mass.
And your own body fat percentage goals can be set based on tools like “Visualize Body Fat Percentage“. Make your goal to achieve a body fat percentage not a goal weight. The goal weight can be determined from the goal body fat percentage, etc.
Here’s some DIY Weightlifting Equipment sites.
JOURNAL OF ANTHROPOLOGICAL ARCHAEOLOGY 2, 1-31 (1983) Energy Source, Protein Metabolism, and Hunter-Gatherer Subsistence Strategies (entire paper as PDF document) JOHN D.
During late winter and spring, hunter-gatherers in temperate, subarctic, and arctic environments often relied on diets that provided marginal or inadequate caloric intakes. During such periods, particularly when stored food supplies dwindled or were used up entirely, lean meat became the principal source of energy. Nutritional problems associated with high-protein, low-energy diets are discussed. These problems include elevated metabolic rates, with correspondingly higher caloric requirements, and deficiencies in essential fatty acids. The relative benefits of adding fat or carbohydrate to a diet of lean meat are evaluated in light of the protein-sparing capacities of these two nutrients. Experimental data indicate that although both enhance high-protein, low-energy diets, carbohydrate is a more effective supplement than fat. Given the nutritional inadequacies of a lean-meat diet, the paper concludes with a discussion of alternative subsistence strategies that increase the availability of carbohydrate or fat at the critical time of year.
Intuitively, we all know that our metabolism slows as we age. Did you though this has been quantified? Here’s the chart of Basal Metabolic Rates in men and women vs age:
So this, at least in part, demonstrates why it is harder at 50 to lose weight than when we are 20. For a man of 20 their BMR is about 46 and the same man (at the same size) their BMR is around 38. That’s only 82% of the age at 20. So, yes, it is harder to lose weight since you have to eat less to lose weight than you did when you were young, but it is not at all impossible.
Even if you are older, you can do it.
In an interesting paper the question is asked what if the history of the development of our understanding of diabetes has it wrong? The paper (J. Denis McGarry. What If Minkowski Had Been Ageusic? An Alternative Angle on Diabetes. Science, Vol. 258, No. 5083 (Oct. 30, 1992), pp. 766-770).
Despite decades of intensive investigation, the basic pathophysiological mechanisms responsible for the metabolic derangements associated with diabetes mellitus have remained elusive. Explored here is the possibility that traditional concepts in this area might have carried the wrong emphasis. It is suggested that the phenomena of insulin resistance
and hyperglycemia might be more readily understood if viewed in the context of underlying abnormalities of lipid metabolism.
Some powerful food for thought in the paper. Another paper (Arius, Energy Metabolism
) summarizes the argument as:
The author considers the possibility that the hyperinsulinemia of early non-insulin—dependent diabetes is coincident with hyperamylinemia, since insulin and amylin are cosecreted. Amylin would cause an increase in plasma lactate (Cori cycle); and lactate, a better precursor than glucose for fatty acid synthesis, would indirectly promote the production of very-low-density lipoproteins (VLDL). There would follow an increased flux of triglycerides from liver to muscle (and adipose tissue) and, as proposed and elaborated on, an increase in insulin resistance and production of many of the metabolic disturbances occurring in diabetes.
The Randle cycle is a biochemical mechanism involving the competition between glucose and fatty acids for their oxidation and uptake in muscle
and adipose tissue
. The cycle controls fuel selection and adapts the substrate supply and demand in normal tissues. This cycle adds a nutrient-mediated fine tuning on top of the more coarse hormonal control on fuel metabolism. This adaptation to nutrient availability applies to the interaction between adipose tissue and muscle. Hormones that control adipose tissue lipolysis affect circulating concentrations of fatty acids, these in turn control the fuel selection in muscle. Mechanisms involved in the Randle Cycle include allosteric control, reversible phosphorylation and the expression of key enzymes. The energy balance from meals composed of differing macronutrient composition is identical, but the glucose and fat balances that contribute to the overall energy balance change reciprocally with meal composition.
Fatty acids may act directly upon the pancreatic β-cell to regulate glucose-stimulated insulin secretion. This effect is biphasic. Initially fatty acids potentiate the effects of glucose. After prolonged exposure to high fatty acid concentrations this changes to an inhibition. Randle suggested that the term fatty acid syndrome would be appropriate to apply to the biochemical syndrome resulting from the high concentration of fatty acids and the relationship to abnormalities of carbohydrate metabolism, including starvation, diabetes and Cushing’s syndrome.
My own weight had been in the 280 range for a long time. In the months before I was diagnosed as Type 2 Diabetic my weight dropped 50 lbs without any lifestyle changes. After I went on Metformin my weight was relatively lower for a while. When I eventually went on Insulin my weight went up 40+ lbs fairly quickly. It is well known that Insulin adds weight.
My own thought is that the Insulin is both the lock and the key. Increased levels of Insulin pushes glucose or fat into cells and decreased levels of Insulin allows fat to come out of cells. That’s why Intermittent Fasting is such a great bullet for Type 2 diabetics. It allows our fasting Insulin levels to drop. Add to that Low Carbohydrate diets and the perfect recipe for controlling Diabetes comes into play.
The problem never really was Insufficient Insulin. The problem was too much Insulin. And clearly it is a fat related problem.
I asked a friend to be part of an experiment which involved him poking himself with a needle most of the morning. And he agreed. We are both fat adapted (me for 15 months and him for more than 6 months).
We both started fasted from the previous night (no breakfast for myself or my friend). We both ingested 50 g of Whey Protein (IsoPure Zero Carb Protein Powder) at the same time and measured our blood sugar responses over the course of the same morning.
I am a Type 2 Diabetic who has their Blood Sugar “under control” via diet and am no longer on meds. I am 57-years old and do some exercise (CrossFit) five times a week for the past two months.
My fried is a Tri-athlete in his mid-30’s. He’s not a Diabetic and runs frequently.
Here’s the two responses to the same amount of Whey Protein:
The results were very interesting.
- His fasted (starting) Blood Sugar number was higher than mine. We’ve compared numbers before and noted this same thing. We did not use the same meter since we were looking for relative differences not absolute values.
- After ingesting Protein, the Tri-athlete’s blood sugar went down. My blood sugar (the Type 2 Diabetic) went up.
- His Blood Sugar returned to normal much more quickly than mine (less than 2 hours. Mine took over three hours to return to normal.
I am not sure if his Blood Sugar went down due to him not having Insulin Resistance. If his Insulin went up in response to the Protein it could have driven his Blood Sugar down. Since I still have some degree of Insulin Resistance my Blood Sugar doesn’t go down nearly as well.
Support for this idea comes from (“Liver Metabolism“):
Overall, gluconeogenesis is stimulated by glucagon and
epinephrine and inhibited by insulin, as observed most
dramatically in insulin-dependent diabetes mellitus, in
which uninhibited gluconeogenesis contributes significantly
to the hyperglycemia.
Insulin favors oxidative decarboxylation of pyruvate and, therefore, also indirectly tends to diminish gluconeogenesis.
High Protein Diets are good at reducing NAFLD (Non-Alcoholic Fatty Liver Disease). From the study (February 2017, Volume 152, Issue 3, Pages 571–585.e8. Isocaloric Diets High in Animal or Plant Protein Reduce Liver Fat and Inflammation in Individuals With Type 2 Diabetes. Mariya Markova, Etc.):
In a prospective study of patients with type 2 diabetes, we found diets high in protein (either animal or plant) significantly reduced liver fat independently of body weight, and reduced markers of insulin resistance and hepatic necroinflammation. The diets appear to mediate these changes via lipolytic and lipogenic pathways in adipose tissue. Negative effects of BCAA or methionine were not detectable. FGF21 level appears to be a marker of metabolic improvement.
And from the conclusions section:
Postprandial levels of BCAAs and methionine were significantly higher in subjects on the AP vs the PP diet. The AP and PP diets each reduced liver fat by 36%−48% within 6 weeks (for AP diet P = .0002; for PP diet P = .001). These reductions were unrelated to change in body weight, but correlated with down-regulation of lipolysis and lipogenic indices. Serum level of FGF21 decreased by 50% in each group (for AP diet P < .0002; for PP diet P < .0002); decrease in FGF21 correlated with loss of hepatic fat. In gene expression analyses of adipose tissue, expression of the FGF21 receptor cofactor β-klotho was associated with reduced expression of genes encoding lipolytic and lipogenic proteins. In patients on each diet, levels of hepatic enzymes and markers of inflammation decreased, insulin sensitivity increased, and serum level of keratin 18 decreased.
Dr Fung makes the following statement on this webpage (Why Low Carb Is High in Fat – Not Protein):
Once again, these amino acids are absorbed into the portal circulation and directed towards the liver where excess amino acids get turned into glucose.
Turns out the process is much more complicated. To be fair Dr Fung may be simplifying the process for his readers, but the process is more like this (which is probably still an oversimplification). From (Amino Acid Metabolism and Synthesis Explained):
Amino acids that are in excess of the body’s needs are converted by liver enzymes into keto acids and urea. Keto acids may be used as sources of energy, converted into glucose, or stored as fat. Urea is excreted from everyone’s body in sweat and urine.
So it is not quite as simple as Dr Fung lays it out. And keto acids are exactly the goal of any Low Carb diet, ie, the production of ketone bodies. We know that the production of glucose from ketones is necessary to feed brain cells (and some other cells) since they don’t get glucose from carbohydrates when we are on a ketogenic diet. In the absence of any dietary carbohydrates we may actually need more Protein to fuel this very path.
Are the Low Protein LCHF folks then making a serious mistake with very low levels of Protein? Are they relying on studies for necessary Protein levels where subject were not in Ketosis? I will bet a donut they are.
What is the basis for “in excess of the body’s needs”? On what timeframe? Is that per day, meal, hour?
The original mission of this BLOG was to find a cure or at least a way of dealing with my own Insulin Resistance. A typical Type 2 Diabetic has Insulin Resistance. I knew that was what it was called but what is Insulin Resistance and how can someone tell if they have Insulin Resistance?
This paper lays out one way to determine if you have Insulin Resistance (Ann Intern Med. 2003 Nov 18;139(10):802-9. Use of metabolic markers to identify overweight individuals who are insulin resistant. McLaughlin T1, Abbasi F, Cheal K, Chu J, Lamendola C, Reaven G.) using the numbers that you typically get when you get your blood work done.
Plasma triglyceride concentration, ratio of triglyceride to high-density lipoprotein cholesterol concentrations, and insulin concentration were the most useful metabolic markers in identifying insulin-resistant individuals. The optimal cut-points were 1.47 mmol/L (130 mg/dL) for triglyceride, 1.8 in SI units (3.0 in traditional units) for the triglyceride-high-density lipoprotein cholesterol ratio, and 109 pmol/L for insulin. Respective sensitivity and specificity for these cut-points were 67%, 64%, and 57% and 71%, 68%, and 85%. Their ability to identify insulin-resistant individuals was similar to the ability of the criteria proposed by the Adult Treatment Panel III to diagnose the metabolic syndrome (sensitivity, 52%, and specificity, 85%).
To summarize (in US units):
- Triglycerides > 130 mg/dL
- Triglyceride to HDL ratio > 3.0 (using US units)
- Insulin > 109 pmol/L
I haven’t ever had my Insulin measured so I don’t know what that number would be but I did have the other numbers done in 2015 and here are my numbers:
- Triglycerides = 460 mg/dL
- HDL Cholesterol = 36
- Ratio = 12.7
Those numbers are well over the numbers that trigger the diagnosis of Insulin Resistance (aka Metabolic Syndrome). Check your own numbers to see where you are.