Active Low-Carber Forums
Atkins diet and low carb discussion provided free for information only, not as medical advice.
Home Plans Tips Recipes Tools Stories Studies Products
Active Low-Carber Forums
A sugar-free zone


Welcome to the Active Low-Carber Forums.
Support for Atkins diet, Protein Power, Neanderthin (Paleo Diet), CAD/CALP, Dr. Bernstein Diabetes Solution and any other healthy low-carb diet or plan, all are welcome in our lowcarb community. Forget starvation and fad diets -- join the healthy eating crowd! You may register by clicking here, it's free!

Go Back   Active Low-Carber Forums > Main Low-Carb Diets Forums & Support > Low-Carb Studies & Research / Media Watch > LC Research/Media
User Name
Password
FAQ Members Calendar Mark Forums Read Search Gallery My P.L.A.N. Survey


Reply
 
Thread Tools Display Modes
  #1   ^
Old Thu, Sep-30-21, 02:26
Demi's Avatar
Demi Demi is offline
Posts: 26,664
 
Plan: Muscle Centric
Stats: 238/153/160 Female 5'10"
BF:
Progress: 109%
Location: UK
Default Study shows low carb diet has no adverse effect on LDL cholesterol levels

Quote:
Effects of a low-carbohydrate diet on insulin-resistant dyslipoproteinemia—a randomized controlled feeding trial

Cara B Ebbeling, Amy Knapp, Ann Johnson, Julia M W Wong, Kimberly F Greco, Clement Ma, Samia Mora, David S Ludwig

Background
Carbohydrate restriction shows promise for diabetes, but concerns regarding high saturated fat content of low-carbohydrate diets limit widespread adoption.

Objectives
This preplanned ancillary study aimed to determine how diets varying widely in carbohydrate and saturated fat affect cardiovascular disease (CVD) risk factors during weight-loss maintenance.

Methods
After 10–14% weight loss on a run-in diet, 164 participants (70% female; BMI = 32.4 ± 4.8 kg/m2) were randomly assigned to 3 weight-loss maintenance diets for 20 wk. The prepared diets contained 20% protein and differed 3-fold in carbohydrate (Carb) and saturated fat as a proportion of energy (Low-Carb: 20% carbohydrate, 21% saturated fat; Moderate-Carb: 40%, 14%; High-Carb: 60%, 7%). Fasting plasma samples were collected prerandomization and at 20 wk. Lipoprotein insulin resistance (LPIR) score was calculated from triglyceride-rich, high-density, and low-density lipoprotein particle (TRL-P, HDL-P, LDL-P) sizes and subfraction concentrations (large/very large TRL-P, large HDL-P, small LDL-P). Other outcomes included lipoprotein(a), triglycerides, HDL cholesterol, LDL cholesterol, adiponectin, and inflammatory markers. Repeated measures ANOVA was used for intention-to-treat analysis.

Results
Retention was 90%. Mean change in LPIR (scale 0–100) differed by diet in a dose-dependent fashion: Low-Carb (–5.3; 95% CI: –9.2, –1.5), Moderate-Carb (–0.02; 95% CI: –4.1, 4.1), High-Carb (3.6; 95% CI: –0.6, 7.7), P = 0.009. Low-Carb also favorably affected lipoprotein(a) [–14.7% (95% CI: –19.5, –9.5), –2.1 (95% CI: –8.2, 4.3), and 0.2 (95% CI: –6.0, 6.8), respectively; P = 0.0005], triglycerides, HDL cholesterol, large/very large TRL-P, large HDL-P, and adiponectin. LDL cholesterol, LDL-P, and inflammatory markers did not differ by diet.

Conclusions
A low-carbohydrate diet, high in saturated fat, improved insulin-resistant dyslipoproteinemia and lipoprotein(a), without adverse effect on LDL cholesterol. Carbohydrate restriction might lower CVD risk independently of body weight, a possibility that warrants study in major multicentered trials powered on hard outcomes.

https://doi.org/10.1093/ajcn/nqab287
Reply With Quote
Sponsored Links
  #2   ^
Old Thu, Sep-30-21, 07:14
wbahn's Avatar
wbahn wbahn is offline
Senior Member
Posts: 8,651
 
Plan: Atkins-ish, post-WLS
Stats: 408.0/288.0/168.0 Male 72 inches
BF:
Progress: 50%
Location: Southern Colorado, USA
Default

While the results are hardly surprising to us that have been around low-carb for any length of time, this study makes the same mistake that so many others do. It considers the "low carb" plan to be one that still has as much carbs as protein (20% of calories for each). For the typical 2000 kcal/day diet, that's 100 g of carbs a day. How many of us would consider that "low carb", even in maintenance, except for people that are extremely physically active?

But at least it is one more study showing that all the "common wisdom" of the last half century is pure nonsense.
Reply With Quote
  #3   ^
Old Thu, Sep-30-21, 09:58
Dodger's Avatar
Dodger Dodger is online now
Posts: 8,758
 
Plan: Paleoish/Keto
Stats: 225/167/175 Male 71.5 inches
BF:18%
Progress: 116%
Location: Longmont, Colorado
Default

This study started in 2014 when eggs were still deadly. The sample diets that they posted showed, for the low carb group, egg white, no yolk, for breakfast which also included orange juice. Lunch was a vegetarian sloppy joe with grapes. Dinner included orange slices. I seemed to be more Mediterranean diet orientated than low-carb.
Certainly, there would have been much better results if the low-carb was much lower in carbs.
Reply With Quote
  #4   ^
Old Thu, Sep-30-21, 10:37
khrussva's Avatar
khrussva khrussva is offline
Say NO to Diabetes!
Posts: 8,671
 
Plan: My own - < 30 net carbs
Stats: 440/228/210 Male 5' 11"
BF:Energy Unleashed
Progress: 92%
Location: Central Virginia - USA
Default

Now that I am metabolically healthy, when I eat a lower carb diet in the 60 to 100 carb range I get stellar cholesterol numbers. My HDL is high, triglycerides are low and my LDL is in a range acceptable to my doctor. But when I eat a very low carb/keto diet (< 20 net carbs) my LDL-C will more than double -- especially if I'm exercising and actively losing weight. In other words, I'm a cholesterol hyper-responder when I do keto. I still have a stellar Triglyceride/HDL ratio, but my TC and LDL-C are off the charts. This is not uncommon, especially for the lean, athletic type Keto people. Dave Feldman has thousands of members on his Lean Mass Hyper Responder Facebook group and the typical first post by new members is all about how they and/or their doctor's are freaking out about LDL-C at 2 or 3 times the max reference range. Doctors typically see this and think that the patient is a ticking time-bomb desperately in need of statin treatment.

Personally, I'm of the belief that this is a normal function of our body for healthy people who are fueled mostly by fat. My doctor begs to differ. An LDL-C of < 120 mg/dl she will accept. On keto my LDL-C can exceed 250 mg/dl. I had to turn down another hard push for a statin prescription just yesterday. It happens with every visit. So maybe it is good that this study was done on "lower carb" participants. They may have had much different conclusions if they had studied a proper keto diet and a bunch of hyper-responders show up in their sample group.

FYI: Dave Feldman managed to get a study funded with the intent to determine if Lean Mass Hyper Responders are at greater risk for heart disease. The study is just now getting underway. Hopefully we will know more at the conclusion of this study. Here is a link to an interview with Dave about this study.

Discussing the LMHR Study on the DD Podcast

Last edited by khrussva : Thu, Sep-30-21 at 13:47.
Reply With Quote
  #5   ^
Old Fri, Oct-01-21, 04:54
JEY100's Avatar
JEY100 JEY100 is offline
Posts: 13,370
 
Plan: P:E/DDF
Stats: 225/150/169 Female 5' 9"
BF:45%/28%/25%
Progress: 134%
Location: NC
Default

Ken, these are brilliant observations. I copied it to add to the thread on Cholesterol and LC Diets…I had similar results and didn’t realize it until now Reading your post. https://forum.lowcarber.org/showthr...919#post9414919
Reply With Quote
  #6   ^
Old Fri, Oct-01-21, 08:06
Demi's Avatar
Demi Demi is offline
Posts: 26,664
 
Plan: Muscle Centric
Stats: 238/153/160 Female 5'10"
BF:
Progress: 109%
Location: UK
Default

Quote:
Do we really know what makes us fat?

We’re familiar with the pattern by now: Every few years, a new study emerges with new obesity statistics. The numbers seem shockingly high, almost impossibly high, until the next study comes along with numbers that are higher still. In the 1970s, approximately 15% of American adults met the obesity criteria. By the end of the 1980s, that 15% had grown to more than 20%. By the year 2000, we had reached 30%. Today, 42% of American adults are classified as obese, and an additional 30% are considered overweight. Whatever is happening, it is happening to a remarkable number of us.

The astonishing increase in obesity has coincided with an equally astonishing increase in diabetes, which has risen approximately 500% over the last 50 years. And diabetes is only the beginning. The obesity epidemic has put tens of millions of Americans at far greater risk for heart attacks, strokes, Alzheimer’s, many of our most deadly cancers and, as we’ve recently learned, dying of COVID-19.

Given the undeniable trend, the most shocking part of the obesity epidemic may be that few health officials or scientific authorities have paused to ask a very simple question: Is it possible that our failure to make any progress stems from a scientific oversight? Is it possible that we have misunderstood obesity this entire time?

The prevailing wisdom on obesity has not gone entirely unchallenged. Over the last two decades, a small but growing number of doctors, scientists and journalists have argued that we have, in fact, fundamentally misunderstood the science of what makes us fat. These challengers have long seemed like underdogs, rebels hurling rocks at a well-fortified scientific dogma.

But that perception may now be changing. This month, Harvard Medical School professor David Ludwig and 16 other prominent scientists, clinical researchers and public health experts published a “perspective” in the American Journal of Clinical Nutrition that spells out the problems with the current model of obesity and puts forward a possible alternative. An overdue scientific reckoning on obesity appears to be taking place.

If we’ve been slow to think in new ways about obesity, it’s probably because the prevailing model — that obesity is a problem of overeating and not exercising enough — seems so obviously true. According to this “energy-balance” obesity model, we get fatter for one simple reason: More calories are coming into our bodies than are going out. In the last decades of the 20th century, the thinking goes, more processed foods infiltrated our grocery stores and our lives. Such foods are engineered to trigger reward signals in our brains, and we end up bingeing on them. Meanwhile, our sedentary lifestyles prevent us from burning enough calories.

The authors of the Clinical Nutrition paper don’t dispute that, if someone is growing heavier, more calories, or energy, are entering that person’s body than leaving it. But, they argue, the energy-balance model only describes what happens as we gain weight; it doesn’t explain why it happens.

Specifically, the model doesn’t tell us why our fat cells are holding on to the calories we consume rather than releasing the energy to fuel the body. After all, our body fat evolved precisely so that we could take in large quantities of food and then release that energy to fuel ourselves when we are not eating. That we are not moving enough doesn’t seem to be the answer. Though moving more is certainly good for us and recommended by virtually all health experts, exercise by itself has not proved especially helpful for losing weight.

So why do we keep gaining so much weight? The Clinical Nutrition article argues that obesity is fundamentally a hormonal and metabolic issue: We become obese because our bodies secrete too much of the hormone insulin, which instructs our fat cells to take up and store fat. Insulin functions like a supervisor at a food warehouse. It directs the trucks dropping off their loads in the warehouse and then locks the doors. Our bodies may have more than enough stored fuel, but if insulin levels remain elevated, the fuel can’t escape our fat tissue to nourish the rest of the body. We begin to feel weak and hungry. And we eat more.

If this understanding of obesity is correct, the energy-balance model has obesity backward: Overeating is a response to growing fatter (that is, to our fat tissues hoarding calories) rather than an underlying cause of growing fatter. Further, whatever raises insulin levels excessively in our blood is likely to be the true culprit in obesity.

In place of the energy-balance model, the Clinical Nutrition article proposes a carbohydrate-insulin model because the pancreas releases more insulin in response to processed carbohydrates than to any other foods. Our obesity epidemic took off in the 1980s, it follows, not simply because we started to eat more calories in the form of processed food, but because we began to replace the healthy fats in our diet with refined sugars and grains.

To appreciate how obesity researchers could have missed the hormonal connection to weight gain for so long, consider that refined sugars and grains, the same molecules that elevate insulin levels, also happen to be a source of calories. The great mistake, according to proponents of the carbohydrate-insulin model, was blaming refined carbohydrates primarily for their energy content, their calories, rather than for their influence on our hormones.

For the public, scientific debates about the nuances of obesity and the way our bodies store and access energy can seem like so much squabbling over minor points. But given the link between obesity and chronic disease, there may be no single question in American life more important than which side of this debate is correct.

If the carbohydrate-insulin model is correct — and its proponents acknowledge that we need more research before saying so with absolute certainty — it suggests a radically different approach to restoring health to the nearly three-quarters of American adults who are overweight. Instead of aiming to eat fewer calories, an approach that follows from the energy-balance model and that has failed for so many of us, we should replace the refined carbohydrates in our diets with healthy fats and protein without much concern for counting calories. Such a high-fat, low-carbohydrate diet would lower insulin levels and allow our fat cells to release the calories they are hoarding.

Whether the debate among scientists leads to a revolution in how we understand the science of getting fat remains to be seen. But if our health experts continue along the same path without reconsidering whether we’ve lost our way, one thing is clear: We’ll know what to expect when the next figures on American obesity are published.

Sam Apple is the author of “Ravenous: Otto Warburg, the Nazis, and the Search for the Cancer-Diet Connection.” He teaches science writing at Johns Hopkins University.


https://www.latimes.com/opinion/sto...n-carbohydrates
Reply With Quote
  #7   ^
Old Fri, Oct-01-21, 08:07
GRB5111's Avatar
GRB5111 GRB5111 is offline
Senior Member
Posts: 4,036
 
Plan: Very LC, Higher Protein
Stats: 227/186/185 Male 6' 0"
BF:
Progress: 98%
Location: Herndon, VA
Default

Quote:
Originally Posted by khrussva
Personally, I'm of the belief that this is a normal function of our body for healthy people who are fueled mostly by fat. My doctor begs to differ. An LDL-C of < 120 mg/dl she will accept. On keto my LDL-C can exceed 250 mg/dl. I had to turn down another hard push for a statin prescription just yesterday. It happens with every visit. So maybe it is good that this study was done on "lower carb" participants. They may have had much different conclusions if they had studied a proper keto diet and a bunch of hyper-responders show up in their sample group.

FYI: Dave Feldman managed to get a study funded with the intent to determine if Lean Mass Hyper Responders are at greater risk for heart disease. The study is just now getting underway. Hopefully we will know more at the conclusion of this study. Here is a link to an interview with Dave about this study.

Ken - agree with your belief. The frustrating issue, ignoring CAC for the moment, is that popular identification of heart disease and risk relies on blood lipids, and I'm concerned, convinced we don't know the whole story. As per Feldman, I can "hack" my lipid panel results to make the doctors comfortable with my results. Do they really indicate I'm healthy? When I fasted for over 4 days before an NMR LipoProfile test a few years ago, did my higher LDL mean I was a walking time bomb or that my metabolism was simply burning my on-board fat for energy? The next test I did a straight 12-hour fast and my lipids were normal. In both tests my triglycerides were very low (low 40s) and my HDL was high (70s). My IR score was extremely low, indicating that I was not in the least insulin resistant. Glad to hear Dave Feldman is pursuing this in a formal study, thanks for the link. All this may simply mean we humans have the ability to adapt to the consumption of energy that is most prevalent at the time, but no one knows the long-term effects. Despite the continued recommendation of lipid guidelines and the massive sales of statins, serious health epidemics persist. We still have much to learn.
Reply With Quote
  #8   ^
Old Fri, Oct-01-21, 08:53
cotonpal's Avatar
cotonpal cotonpal is online now
Senior Member
Posts: 5,283
 
Plan: very low carb real food
Stats: 245/125/135 Female 62
BF:
Progress: 109%
Location: Vermont
Default

My way around all this is to simply not get my cholesterol levels checked. It's probably been at least 2 decades. I simply told my doctor that since I had no plans to take a statin and no plans to change my diet there was no reason to get the blood tests to check the level. After a few years she gave up asking me. I rely on my healthy eating habits long with a bit of exercise to keep as healthy as possible.
Reply With Quote
  #9   ^
Old Sat, Oct-02-21, 04:09
WereBear's Avatar
WereBear WereBear is offline
Senior Member
Posts: 14,606
 
Plan: EpiPaleo/Primal/LowOx
Stats: 220/125/150 Female 67
BF:
Progress: 136%
Location: USA
Default

Quote:
Originally Posted by cotonpal
My way around all this is to simply not get my cholesterol levels checked. It's probably been at least 2 decades. I simply told my doctor that since I had no plans to take a statin and no plans to change my diet there was no reason to get the blood tests to check the level. After a few years she gave up asking me. I rely on my healthy eating habits long with a bit of exercise to keep as healthy as possible.


It's a fine move. It also indicates how hard doctors have been trained to push the statins. Which I think also interferes with how the side effects picture has been slammed shut. I've seen all the aches, pains, memory, and mental issues shoved under the rug of "You're old, get used to it."

No. I don't want to get used to it if there's something I can DO.

From 2016:

Quote:
Systematic review of studies of over 68,000 elderly people also raises questions about the benefits of statin drug treatments

Diamond also points out the research that suggests that high cholesterol may be protective against diseases which are common in the elderly. For example, high levels of cholesterol are associated with a lower rate of neurological disorders, such as Parkinson's disease and Alzheimer's disease. Other studies have suggested that high LDL-C may protect against some often fatal diseases, such as cancer and infectious diseases, and that having low LDL-C may increase one's susceptibility to these diseases.

No association between 'bad cholesterol' and elderly deaths
Reply With Quote
Reply

Thread Tools
Display Modes

Posting Rules
You may not post new threads
You may not post replies
You may not post attachments
You may not edit your posts

vB code is On
Smilies are On
[IMG] code is On
HTML code is Off



All times are GMT -6. The time now is 19:09.


Copyright © 2000-2024 Active Low-Carber Forums @ forum.lowcarber.org
Powered by: vBulletin, Copyright ©2000 - 2024, Jelsoft Enterprises Ltd.