How to lose 93 pounds of baby weight in a year

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Recently I received an e-mail from Hanna Uutela. She had gained a lot of weight during two pregnancies, and was 254 lbs (115 kg) to match her  5′ 3″ (160 cm) stature at the time her second son was born. In addition, she had suffered from daily IBS issues most of her life.

Here’s what happened when she adopted an LCHF diet:

The Email

Hi Andreas!

I’d like to let people know about my weight journey and health improvements, that I’ve experienced during the last two years.

I became severely overweight in 2009, as I was expecting our first child. I gained about 77 lbs (35 kg). The day our son was born, the scale hit 249 lbs (113 kg), and I’m just 5′ 3″ (160 cm) short. With my pregnancy I also had heel pain and sciatic nerve pain, and for sixteen years I had suffered from IBS daily.

I didn’t succeed in losing weight, despite various “healthy” diets. In 2010 I was 207 lbs (94 kg) and started an LCHF diet for the first time. In five weeks I lost 24 lbs (11 kg), without any exercise. The inflammation in my heels went away before I even had time to notice.

After having reached 183 lbs (83 kg) I got pregnant again. I planned to continue my LCHF diet during my pregnancy, but had so much nausea that I just couldn’t do it. On the day that our second son was born (in May 2011), I weighed 254 lbs (115 kg). Once again, my whole body ached. I started to gradually reduce sugar and carbohydrate intake, but didn’t start LCHF seriously, or exercising, until in November that year.

In a year, I lost 97 lbs (42 kg). By the second day my IBS disappeared, and so did the inflammations in my heels. I haven’t had any stomach pain since I began to eat an LCHF diet. I’ve never felt this great before!

Due to both rapid weight gain and rapid weight loss, my skin didn’t really keep up so I had a tummy tuck done in March 2013, where they removed loose skin that I still carried from losing all that weight. So I’ve lost 97 lbs (42 kg) in a year and this past year my body has reshaped itself without any further weight loss. I’m exactly where I want to be.

By now I’ve been on an LCHF diet for two years and wouldn’t dream of changing it for the world.

Sincerely // Hanna Uutela

Congratulations, Hanna!

You can follow Uutela’s journey on her blog: From fat to hot (Google translated from Swedish)

PS

Do you have a success story you want to share on this blog? Send it (photos appreciated) to andreas@dietdoctor.com. Let me know if it’s OK to publish your photo and name or if you’d rather remain anonymous.

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17 comments

  1. Sherry
    Congratulations, several times over, Hanna!
    The weight loss was phenomenal. It must be marvelous
    to be cured after a life-long struggle with Irritable Bowel Syndrome.
    I'm sure your husband and the little boys are fun, too.
    Best wishes for you and your young family!
  2. kevin mulder
    Ketogenic diets provide weightloss,
    but do they also promote healthy kidneys?

    I've been reading for hours about the effect of ketosis on the kidneys,
    and it seems like they heavily increase the likelyhood of developing kidney stones.

    Search google for "children seizures ketogenic diet" and you will get to see websites that refer to recent scientific studies where Epileptic Children on the Ketogenic Diet have 500 times more chance of having kidney stones than children who dont.

    For that reason they need to supplement their diet with not only a lot of water but also with special supplements to prevent/combat kidneysstones.

    Replies: #3, #4
  3. Zepp
    Noe.. its not about ketogenic diet.. its about any diet.. and ketogenic diet for epilepsy is a harch diet.. restricted of almoste anything and low in calories!

    "This study provides preliminary evidence that long-term weight loss with a very-low-carbohydrate diet does not adversely affect renal function compared with a high-carbohydrate diet in obese individuals with normal renal function."

    http://www.ncbi.nlm.nih.gov/pubmed/20338292

    http://site.matthewsfriends.org/uploads/File/StonesPolycitra1.pdf

  4. Paul the rat
    Well, I am sure that there are number of bloggers here who are long-term LCHF-ers.

    Let us hear if anyone has any kidney issues -

    Personally, I check my body physiology thoroughly with regular intervals. After several years of LCHF with minimal carbohydrate intake (often less than 5% energy) my kidneys biochemical signature is that of healthy 20-something (and I know what I was doing when JFK was assassinated).

  5. kevin mulder
    http://perfecthealthdiet.com/2010/11/dangers-of-zero-carb-diets-iv-ki...

    I think the extensive research on these kids seems to prove that a ketogenic diet at least increases likelyhood on developing kidneystones.

    Most people who are keeping their carbs above 60grams per day will not reach a state of ketosis so for them theres no added risk.

    Yet this site routinely advises people to seek out ketogenoc dieting below 50g,
    And it blows my mind that not a single of caution about kidney stones are added to it.

    Reply: #6
  6. Paul the rat
    Fatty acids are preferred energy source for kidneys (amongst all other organs). How something which is preferred be detrimental?. Some children on KD do get kidney stones - this is due to badly designed and implemented KD.

    I repeat my question - does anyone who follow LCHF for a long time have kidney problem ?

    Reprod Nutr Dev. 1985;25(1B):303-19.
    Fatty acid oxidation and ketogenesis during development.
    Girard J, Duée PH, Ferré P, Pégorier JP, Escriva F, Decaux JF.
    Abstract

    Fatty acids are the preferred oxidative substrates of the heart, skeletal muscles, kidney cortex and liver in adult mammals.

    They are supplied to these tissues either as nonesterified fatty acids (NEFA), or as triglycerides after hydrolysis by lipoprotein lipase. During fetal life, tissue capacity to oxidize NEFA is very low, even in species in which the placental transfer of NEFA and carnitine is high. At birth, the ability to oxidize NEFA from endogenous sources or from milk (a high-fat diet) develops rapidly in various tissues and remains very high throughout the suckling period. Ketogenesis appears in the liver by 6 to 12 hrs after birth, and the ketone bodies are used as oxidative fuels by various tissues during the suckling period. At the time of weaning, the transition from a high-fat to a high-carbohydrate diet is attended by a progressive decrease in the ketogenic capacity of the liver, whereas other tissues (skeletal muscle, heart, kidney) maintain a high capacity for NEFA oxidation. The nutritional and hormonal factors involved in changes in fatty acid oxidation during development are discussed.

    Reply: #7
  7. Paul the rat
    What I mean by badly designed ketogenic diet is this: today most physicians are 100% convinced that saturated animal fats are killing us, so they design ketogenic diets based on unsaturated plant oils or hydrogenated oils. Plant oils are disaster not only for kidneys but foremost for the gut function (and hydrogenated oils are more poisonous than cigarette smoke).

    The LCHF diet proposed by dr Eenfeldt is based on animal fats - fats our bodies evolved to utilize as the prime energy source. Personally I do not take more than 3% energy as plant/fish oils.

  8. kevin mulder
    I don't think there is any proof that the higher prevelance of kidneystones among these kids,
    is because they are not eating enough saturated fat. I have read of people on LCHF blogs that they have personally had kidneystones when they were going Ketogenic.

    On sites like these, at least a word of caution and some warnings,
    should be appropriate.

    For example the whole saturated fat thing.
    For most people it creates better HDL/LDL profiles,
    but a small percentage - which is still a big amount of people - have adverse reactions.

    Here's a great article by a pro LCHF cardiologist who warns about the dangers of saturated fats to some people.
    http://blog.trackyourplaque.com/2011/08/diet-one-size-does-not-fit-al...

    A

    Reply: #9
  9. Zepp
    I do think its becuse they are geneticaly predisposal for calciuremia.. and whit a more acidifyed urine they got stones easyer!

    And that what I mean is for any diet, if one got a genetic predisposal for something an changer to ones diet could be that singel step that make one get that bad outcome!

    The easy way to alkalise ones urin is to take that morning glas of orange juice.. but they cant do that.. its to much carbs.. so they provide some other citrates to them!

    And you should know that we have stumbeled on people that have genticaly problems whit fats too.. its not comon but there is those!

    Well its this problem that there are people with geneticaly disturbances.. some cant even eat meat, or fructose.. or fish or other things.. they are rare!

    But one major problem today is that there are more and more people that ingest to much higly digestible carbs and eating too little real food!

    http://articles.latimes.com/2010/dec/20/health/la-he-carbs-20101220

  10. Dana
    Enough of the anti-LC concern trolling.

    Kidney stones vs no kidney stones

    and

    good renal function vs poor renal function

    are two entirely different matters. Apples and oranges.

    A little trip around WebMD would have told you that, Paul, for crying out loud.

    No one *wants* kidney stones, but no one's dying from them, either. Poor renal function, on the other hand... *shrug*

    Replies: #12, #13, #14
  11. Dana
    Also, the way you alkalyze your urine is by your kidneys functioning the way your kidneys already do. They already do the job. You don't need orange juice or calcium tablets for that. Just having enough glutamine in your system will do the trick: your kidneys use that as a buffering agent. It's present in large amounts in meat, you make your own, and you can also supplement it if you are so inclined.

    I would actually *not* want to encourage my body to do a lot of buffering with calcium if I were already prone to stones. You know, that doesn't really make a lot of sense.

  12. Paul the rat
    "...A little trip around WebMD would have told you that, Paul, for crying out loud…."

    1. I am long term LCHF-er, so I am not the one who is anti-LCFH troller, you confused bloggers. Please pay attention to what you read.

    2. In my comments I did not go into the details why kidney stones might be or might be not formed under ketogenic diet, so I did not need to compare oranges with apples or apples with apples.

    3. I use PubMed for my work.

  13. Paul the rat
    "…..but no one's dying from them, either"

    Really ??. Please come over, we go to Urology Dept. I show you the records.

  14. Paul the rat
    @ Dana
    As an example; kidneys synthesize number of proteins which inhibit crystal growth thus stones formation. The rate of synthesis of these proteins (say mg/time) is influenced by genetics and environmental factors (diet). It has been shown that quality of energy used by kidneys as a fuel (glucose, fatty acids, protein) play significant role in biogenesis of these proteins.

    Now, for crying out loud, how this renal function (good = more stone-forming inhibiting proteins or bad = less stone-forming inhibiting proteins) does not correlate with kidney stones formation?.
    Which are apples and which are oranges ?

    Urol Res. 1995;23(5):327-34.

    Identification of a macromolecular crystal growth inhibitor in human urine as osteopontin.

    Sørensen S, Justesen SJ, Johnsen AH.
    Author information

    Abstract
    Macromolecules occurring in human urine inhibit the growth and/or aggregation of calcium oxalate crystals and may prevent the formation of kidney stones. Attention has focused particularly on proteins, as these seem to be most responsible for the inhibitory activity; three proteins, nephrocalcin, an unidentified protein rich in uronic acid, and uropontin have all been described as possessing such activity. We have recently isolated an unknown inhibitor of calcium oxalate crystal growth that co-eluted with trypsin inhibitor in several separation steps, which suggested its identity. The aim of the present study was to outline a simple procedure for isolating and identifying this inhibitor. Purification was done as follows: precipitation of the major proteins (albumin and uromucoid) with trichloroacetic acid, followed by anion exchange chromatography, hydroxyapatite chromatography, anion exchange chromatography, negative affinity chromatography, and twice reversed phase chromatographies of the supernatant. By this procedure, the inhibitor was identified as being a fragment of osteopontin; urinary trypsin inhibitor and nucleic acids were excluded as being responsible for inhibitory action.

  15. Paul the rat
    Langmuir. 2013 May 28;29(21):6287-95. doi: 10.1021/la400891b. Epub 2013 May 16.

    Reversible inhibition of calcium oxalate monohydrate growth by an osteopontin phosphopeptide.

    Nene SS, Hunter GK, Goldberg HA, Hutter JL.
    Author information

    Abstract
    Calcium oxalate, primarily as calcium oxalate monohydrate (COM), is the primary constituent of most kidney stones. Certain proteins, such as osteopontin (OPN), inhibit stone formation. The complexity of stone formation and the effects of urinary proteins at various stages of the process make it hard to predict the exact physiological roles of these proteins in growth inhibition. The inhibition of crystallization due to adsorbed impurities is usually explained in terms of a model proposed in 1958 by Cabrera and Vermilyea. In this model, impurities adsorb to growth faces and pin growth steps, forcing them to curve, thus impeding their progress via the Gibbs-Thomson effect. To determine the role of OPN in the biomineralization of kidney stones, crystal growth on the {010} face of COM was examined in real time with atomic force microscopy in the presence of a synthetic peptide corresponding to amino acids 65-80 (hereafter referred to as pOPAR) of rat bone OPN. We observed clear changes in the morphology of the growth-step structure and a decrease in step velocity upon addition of pOPAR, which suggest adsorption of inhibitors on the {010} growth hillocks. Experiments in which pOPAR was replaced in the growth cell by a supersaturated solution showed that COM hillocks are able to fully recover to their preinhibited state. Our results suggest that recovery occurs through incorporation of the peptide into the growing crystal, rather than by, e.g., desorption from the growth face. This work provides new insights into the mechanism by which crystal growth is inhibited by adsorbants, with important implications for the design of therapeutic agents for kidney stone disease and other forms of pathological calcification.

  16. Brenda Hanson
    News flash...people NOT on a ketogenic diet develop kidney stones.
    Reply: #17
  17. Paul the rat
    There are on average 4-5 admissions every day of people with renal colic to every hospital and these people can be cured with appropriately designed (taking into consideration their particular renal physiology) ketogenic diet.

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