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Share your storyLosing 100 lbs in a year with LCHF
in Success stories 
I received an e-mail from Bengt Nilsson, who’s been on an LCHF diet for a year. Here’s what happened:
The E-mail
Hi Andreas
Thank you for your terrific website, which has inspired me a lot.
The first picture is from November 2012 and the other one was taken today.
With the help of your recommendations I’ve now reached my goal weight, 187 lbs (85 kg). I haven’t followed them to the letter, as I’ve been at 50-75 g carbs/day, but have a very large intake of “good” fats at 150-200 g per day and about the same amount of protein. Almost all carbohydrates come from vegetables, and I eat on average almost 1 kg (2 lbs) daily. I’ve enjoyed keeping a food diary (Dumbbell) and after 11 months my numbers are roughly as stated above. Around 2500-2800 kcal/day, if anyone wants to think about calories.
I do an average of 45 minutes of exercise/weight training per day.
The only extreme part of my diet is probably my egg consumption. I eat about 200 eggs a month in all forms, I never get tired of them and there’s hardly a better food.
I have a friend who is a physician and he’s done my blood work three times during this time. I have no bad health markers, on the contrary. In addition, I feel fantastic and have not been sick during these past 11 months, nor have I had any headaches or stomach pains, I’ve just simply felt great.
I will of course continue to eat like this, but will have to admit that it’s a bit sad that “the journey is over”. I’ve felt fantastic, eaten until satisfied when I was hungry, regardless of time of the day.
I’ve read the entire report from SBU (The Swedish Council on Health Technology Assessment) and I really hope it will get more attention from the media than it has so far.
Sincerely,
Bengt Nilsson
Congratulations, Bengt!
Again well done!
A low-carbohydrate/high-fat diet reduces blood pressure in spontaneously hypertensive rats without deleterious changes in insulin resistance.
Bosse JD, Lin HY, Sloan C, Zhang QJ, Abel ED, Pereira TJ, Dolinsky VW, Symons JD, Jalili T.
Source
Division of Nutrition, University of Utah, Salt Lake City, UT 84112, USA.
Abstract
Previous studies reported that diets high in simple carbohydrates could increase blood pressure in rodents. We hypothesized that the converse, a low-carbohydrate/high-fat diet, might reduce blood pressure. Six-week-old spontaneously hypertensive rats (SHR; n = 54) and Wistar-Kyoto rats (WKY; n = 53, normotensive control) were fed either a control diet (C; 10% fat, 70% carbohydrate, 20% protein) or a low-carbohydrate/high-fat diet (HF; 20% carbohydrate, 60% fat, 20% protein). After 10 wk, SHR-HF had lower (P < 0.05) mean arterial pressure than SHR-C (148 ± 3 vs. 159 ± 3 mmHg) but a similar degree of cardiac hypertrophy (33.4 ± 0.4 vs. 33.1 ± 0.4 heart weight/tibia length, mg/mm). Mesenteric arteries and the entire aorta were used to assess vascular function and endothelial nitric oxide synthase (eNOS) signaling, respectively. Endothelium-dependent (acetylcholine) relaxation of mesenteric arteries was improved (P < 0.05) in SHR-HF vs. SHR-C, whereas contraction (potassium chloride, phenylephrine) was reduced (P < 0.05). Phosphorylation of eNOSSer1177 increased (P < 0.05) in arteries from SHR-HF vs. SHR-C. Plasma glucose, insulin, and homoeostatic model of insulin assessment were lower (P < 0.05) in SHR-HF vs. SHR-C, whereas peripheral insulin sensitivity (insulin tolerance test) was similar. After a 10-h fast, insulin stimulation (2 U/kg ip) increased (P < 0.05) phosphorylation of AktSer473 and S6 in heart and gastrocnemius similarly in SHR-C vs. SHR-HF.
In conclusion, a low-carbohydrate/high-fat diet reduced blood pressure and improved arterial function in SHR without producing signs of insulin resistance or altering insulin-mediated signaling in the heart, skeletal muscle, or vasculature.
KEYWORDS:
Check this out to find the answer to your question.
http://keto-calculator.ankerl.com/
I visited the link you provided. It all seems to be pertaining to calorie counting. Perhaps I misinterpreted the information. Lots of time I find that LCHF sites, books, and lectures reference calorie counting to make a point. This all gets confusing of course. Thank you.
Play a long a litle time and adjust so its seems to be sustaineble.. or rely on that your apetite make the right counting for you.. the last is best and more comfortable.
The amounts of fat one should eat is up to your energy limit.. after you got all other essentiall macro and micro nutrients!
I'd go further and suggest that the endless repetition of this tautology is not just unhelpful but that it has been (and continues to be) harmful to the health of a great many. It takes the focus away from _why_ we unconsciously and consciously are driven to eat anything... it is not a question of maths but of biochemistry.
High carb -> Weight gain
people believe LCHF is some kind of magic where they can just leave out the carbs they can eat limitless and still lose weight. This is simply false, it does not work that way.
In reality it is more like
High carb -> More hunger -> Caloric surplus -> Weight gain.
So high carbs lead to a caloric surplus which is the same as weight gain. If you fix your carb intake and still don't lose weight, there has to be another reason for the caloric surplus.
For the record I do not simplify it to "High carb -> Weight gain", nor do I see Dr Andreas doing any such thing.
(p.s. by the way, I love the term "nutrients dense diet" used by 55/30/15% nutritionists and health gurus. What can be more nutrients dense than say, 100 g of liver + 2 tablespoons of lard + touch of vegetables?)
Eur J Clin Nutr. 2013 Jul;67(7):759-64. doi: 10.1038/ejcn.2013.90. Epub 2013 May 1.
Ketosis and appetite-mediating nutrients and hormones after weight loss.
Sumithran P, Prendergast LA, Delbridge E, Purcell K, Shulkes A, Kriketos A, Proietto J.
Source
Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia.
Abstract
BACKGROUND/OBJECTIVES:
Diet-induced weight loss is accompanied by compensatory changes, which increase appetite and encourage weight regain. There is some evidence that ketogenic diets suppress appetite. The objective is to examine the effect of ketosis on a number of circulating factors involved in appetite regulation, following diet-induced weight loss.
SUBJECTS/METHODS:
Of 50 non-diabetic overweight or obese subjects who began the study, 39 completed an 8-week ketogenic very-low-energy diet (VLED), followed by 2 weeks of reintroduction of foods. Following weight loss, circulating concentrations of glucose, insulin, non-esterified fatty acids (NEFA), β-hydroxybutyrate (BHB), leptin, gastrointestinal hormones and subjective ratings of appetite were compared when subjects were ketotic, and after refeeding.
RESULTS:
During the ketogenic VLED, subjects lost 13% of initial weight and fasting BHB increased from (mean±s.e.m.) 0.07±0.00 to 0.48±0.07 mmol/l (P<0.001). BHB fell to 0.19±0.03 mmol/l after 2 weeks of refeeding (P<0.001 compared with week 8). When participants were ketotic, the weight loss induced increase in ghrelin was suppressed. Glucose and NEFA were higher, and amylin, leptin and subjective ratings of appetite were lower at week 8 than after referring.
CONCLUSIONS:
The circulating concentrations of several hormones and nutrients which influence appetite were altered after weight loss induced by a ketogenic diet, compared with after refeeding. The increase in circulating ghrelin and subjective appetite which accompany dietary weight reduction were mitigated when weight-reduced participants were ketotic.