question about carbs

Sorry, MyFitnessPal folks,

Just found some evidence at bodybuilding.com that certain users (you'll guess which) have been gloating on threads there about their successful trolling here. They should disappear shortly.

Thanks for your patience,
Steven
MyFitnessPal Staff

Sorry if this has already been answered but I couldn't see it. How many carbs is considered low carb? I've been trying to cut out carbs, but I seem to always have about 100g a day! Most of it comes from the fruits & veg I eat, as well as milk that I have with my coffee (which I simply can't live without!) If I am aiming to go mostly low carb (and sort of low GI) should I be cutting down on that? I could try my coffee black.

Personally I aim for the 100g mark on average. If I'm going to have a higher carb day I try to make it on a day I've worked out. I think if your carbs are coming from veggies, fruits, and some dairy, it really doesn't matter whether you're over 100g or not though. Sounds like you're doing fine to me.

Is it working for you?

You are such a jerk. And you obviously didn't even read my post. I DID NOT discount having to consume less when trying to lose weight, just that it's easier if you go about it by eating fewer carbs.

Plus, everything I wrote about insulin is proven science. Look it up, I'm pretty sure that's how it works.

Other than that, I'm over this thread. It's not like I researched a reason to be extra unhealthy. I spend A LOT (probably too much) time researching this stuff because I love it. I started in February, and I didn't discover Paleo until early August. I'm just doing what I honestly think is best for me from EVERYTHING that I've learned thus far. So I give up. I will not be treated like an idiot.

No need to resort to name-calling or getting defensive. I don't think anything Untz has said has been mean, and he hasn't called you a name either though you have now resorted to doing exactly that by calling him a jerk. If you want to tout a low-carb lifestyle and claim that this is fitting for everyone, you should be prepared with peer-reviewed research from unbiased and competently-executed studies to back it up. People have the right to challenge your opinions on a public forum even if you don't like it.

Correction: Your comment was directed at Hunter. Again, I still think it's inappropriate to call him a jerk.

In fairness though, no one here has presented ANY peer-reviewed research to back up thier arguments. The best I've seen in the way of support has been some articles by Lyle which have a very vague relation to the point that was attempting to be made.

I'm certainly not defending or condoning the name-calling, I'm just saying that you are asking for a standard that no one is following.

Personally, I'd love to see some support of the arguements, instead of just people stating things as fact. I really like the debate, until it gets personal and rude, and when it includes supported statements. I know I have my opinion on this topic, but I'd really like to find something to prove me wrong if I am wrong. In short, I'd really like to learn something from the debate.

I consider under 80g to be low carb. When I cycle them I try to stay under 50g on low days although it doesn't matter honestly.

I would definitely consider under 50g to be low carbs, and I've read that ketosis can start with sustained intake of 75g or less.

Yea Tim. Just depends on the tolerance level of a person. It took me 4 days of eating under 30g of carbs to get traces of ketones. Although I don't trust the sticks so much. Not convinced on their accuracy.

To sum it up in short; so long as your overall daily intake of calorie is below your maintenance/base calorie level (the amount of calories you must eat in order to not gain or lose weight) than you will continue to lose weight. Now, how much under this baseline is what determines the amount of weight you will lose.

de novo lipogenesis:

When we talk about the fat stored in the adipose tissue or the fats in our food, we’re talking about triglycerides. Oleic acid, the monounsaturated fat of olive oil, is a fatty acid, but it is present in oils and meats in the form of a triglyceride. Each triglyceride molecule is composed of three fatty acids (the “tri”), linked together on a backbone of glycerol (the “glyceride”). Some of the triglycerides in our fat tissue come from fat in our diet. The rest come from carbohydrates, from a process known as de novo lipogenesis, which is Latin for “the new creation of fat,” a process that takes place both in the liver and, to a lesser extent, in the fat tissue itself. The more carbohydrates flooding the circulation after a meal, the more will be converted to triglycerides and stored as fat for future use (perhaps 30 percent of the carbohydrates in any one meal). “This lipogenesis is regulated by the state of nutrition,” explained Wertheimer in an introductory chapter to the Handbook of Physiology: “it is decreased to a minimum in carbohydrate deficiency and accelerated considerably during carbohydrate availability.”* (*Synthesis of the enzymes required to convert carbohydrates into fat will also increase and decrease in proportion to the carbohydrate content of the diet.)

sorry this is long.

This brings us to the mechanisms that control and regulate the availability of fat and carbohydrates for fuel and regulate our blood sugar in the process.
The first is the triglycerides/fatty-acid cycle we just discussed. This cycle is regulated by the amount of blood sugar made available to the fat tissue. If blood sugar is ebbing, the amount of glucose transported into the fat tissue will decrease; this limits the burning of glucose for energy, which in turn reduces the amount of glycerol phosphate produced. With less glycerol phosphate present, fewer fatty acids are bound up in triglycerides, and more of them remain free to escape into the circulation. As a result, the fatty-acid concentration in the bloodstream increases. The bottom line: as the blood-sugar levels decreases, fatty-acid levels rise to compensate.
If blood-sugar levels increase – say, after a meal containing carbohydrates – then more glucose is transported into the fat cells, which increases the use of this glucose for fuel, and so increases the production of glycerol phosphate. This in turn increases the conversion of fatty acids into triglycerides, so that they’re unable to escape into the bloodstream at a time when they’re not needed. Thus, elevating blood sugar serves to decrease the concentration of fatty acids in the blood, and to increase the accumulated fat in the fat cells.
The second mechanism that works to regulate the availability of fuel and to maintain blood sugar at a healthy level is called the glucose/fatty acid cycle, or the Randle cycle, after the British biochemist Sir Philip Randle. It works like this: As blood-sugar levels decrease – after a meal has been digested – more fatty acids will be mobilized from the fat cells, as we just discussed, raising the fatty-acid level in the bloodstream. This leads to a series of reactions in the muscle cells that inhibit the use of glucose for fuel and substitute fatty acids instead. Fatty acids generate the necessary cellular energy, and the blood-sugar in the circulation stabilizes. When the availability of fatty acids in the blood diminishes, as would be the case when blood-sugar levels are rising, the cells compensate by burning more blood sugar. So increasing blood-sugar levels decreases fatty-acid levels in the blood stream, which in turn increases glucose use in the cells. Blood-sugar levels always remain within safe limits – not too high or too low.
These two cycles are the fundamental mechanisms that maintain and ensure a steady fuel supply to our cells. They provide a “metabolic flexibility” that allows us to burn carbohydrates (glucose) when they’re present in the diet, and fatty acids when they’re not. And it’s the cells of the adipose tissue that function as the ultimate control mechanism of this fuel supply.
Regulation by hormones and the nervous system is then layered onto these baseline mechanisms to deal with the vageries of the external environment, providing the moment-to-moment and season-to-season fine-tuning necessary for the body to work at maximum efficiency. Hormones modify this flow of fatty acids back and forth across the membranes of the fat cells, and they modify the expenditure of energy by the tissues and organs, Hormones, and particularly insulin – “even in trace amounts,” as Ernst Wertheimer explained – “have powerful direct effect on adipose tissue.”
With the invention by Rosalyn Yalow and Solomon Berson of their radioimmunoassay to measure insulin levels, it quickly became clear that insulin was what Yalow and Berson called “the principal regulator of fat metabolism.” Insulin stimulates the transport of glucose into the fat cells, thereby effectively controlling the production of glycerol phosphate, the fixing of free fatty acids as triglycerides, and all that follows. The one fundamental requirement to increase the flow of fatty acids out of adipose tissue – to increase lipolysis – and so decrease the amount of fat in our fat tissue, is to lower the concentration of insulin in the bloodstream. In other words, the release of fatty acids from the fat cells and their diffusion into the circulation require “only the negative stimulus of insulin deficiency,” as Yalow and Berson wrote. By the same token, the one necessary requirement to shut down fat release of fat from the fat cells and increase fat accumulation is the presence of insulin. When insulin is secreted, or the level of insulin in the circulation is abnormally elevated, fat accumulates in the fat tissue. When insulin levels are low, fat escapes from the fat tissue, and the fat deposits shrink.
All other hormones will work to release fatty acids from the fat tissue, but the ability of these hormones to accomplish this job is suppressed almost entirely by the effect of insulin and blood sugar. These hormones can mobilize fat from the adipose tissue only when insulin levels are low – during starvation, or when the diet being consumed is lacking in carbohydrates. (If insulin levels are high, that implies that there is plenty of carbohydrate fuel available.) If fact, virtually anything that increases the secretion of insulin will also suppress the secretion of hormones that release fat from the fat tissue. Eating carbohydrates, for example, not only elevated insulin but inhibits growth-hormone secretion; both effects lead to greater fatty-acid storage in the fat tissue.


Hormones that promote fat metabolism: Epinephrine, Norepinephrine, Adrenocorticotropic hormone (ACTH), Glucagon, Thyroid-stimulating hormone, Melanocyte-stimulating hormone, Vasopressin, Growth hormone

Hormones that promote fat accumulation: Insulin

In 1965, hormonal regulation of adipose tissue looked like this: at least eight hormones that worked to release fat from the adipose tissue and one, insulin, which worked to put it there.

That increasing the secretion of insulin can in fact cause obesity (i.e. excess fat accumulation) would be demonstrated conclusively in animal models of obesity, particularly in the line of research we discussed in chapter 21 on rats and mice with lesions in the area of the brain known as the ventromedial hypothalamus, or VMH. In the 1960s, this research became another beneficiary of Yalow’s and Berson’s new technology to measure circulating levels if insulin. As investigators now reported, insulin secretion in VMH-lesioned animals increases dramatically within seconds of the surgery. The insulin response to eating also goes “off the scale” with the very first meal. The more insulin secreted in the days after the surgery, the greater the ensuing obesity. Obesity in these lesioned animals could be prevented by short-circuiting the exaggerated insulin response – by severing the vagus nerve, for example, that links the hypothalamus with the pancreas.* (*For this reason, vagotomy, as this surgical procedure is known, was later considered a potential treatment for obese humans with various syndromes of hypothalamic obesity.) Similarly, the hypersecretion of insulin was reported to bet the earliest detectable abnormality in genetic strains of obesity-prone mice and rats.
By the mid-1970s, it was clear that Stephen Ranson’s insights into obesity in these animals had been confirmed. The lesion causes a defect in the part of the hypothalamus that regulates what researchers have come to call fuel partitioning – the result is the hypersecretion of insulin. The insulin forces the accumulation of fat in the fat tissue, and the animal overeats to compensate. This research refuted John Brobeck’s notion, which has since become the standard wisdom in the field. That the VMH lesion causes overeating directly and the animals grow fat simply because they eat too much. These studies were neither ambiguous nor controversial. In 1976, University of Washington investigators Stephen woods and Dan Porte described as “overwhelming” the evidence that the increased secretion of insulin is the primary effect of VMH lesions, the driving force of obesity in these animals.

I have gained fat while on a calorie deficit because I started eating too many carbs. I always eat in a calorie deficit. As long as I stay low-carb (actually no grains or sugars - that includes fruit since fructose isn't used as energy at all - it gets sent to the liver and converted to fat) my body fat stays stable no matter how much fat I consume - or calories. I have found it impossible to "overeat" with a high-fat, low-carb lifestyle. The moment I start going higher-carb the body fat % starts to creep up again regardless of how many calories I am consuming. The number on the scale goes up faster because my body will also start retaining too much water since carbs also cause quite a bit of water retention.

My carb addiction is an ongoing battle so I have been watching this happen.

Your personal experience may be due to several factors that are not directly caused by "eating too many carbs". A person's fitness goals and general daily energy expenditure all play into this. For instance, a typical pro cyclist eats 3,000 calories worth of carbohydrates daily to fuel his/her energy expenditure and has 6-10% BF.

Your results with a "low carb lifestyle" may not translate to other people's lifestyles. Take my case. I'm trying to increase my fitness so that I can do hut to hut trip in the Canadian Rockies this winter. This will be a week on touring skis with 10,000 vertical feet of climbing per day to ski powder lines. I'm going with guys and gals 20 years my junior and I need to be in shape to do it. My diet and exercise is critical to meet those late January goals.

Body composition is frankly not that important to me. My focus is on fueling workouts to maximize my cardiovascular-respiratory system. See www.selkirkexperience.com/ski_main.html

I have gained fat while on a calorie deficit because I started eating too many carbs. I always eat in a calorie deficit. As long as I stay low-carb (actually no grains or sugars - that includes fruit since fructose isn't used as energy at all - it gets sent to the liver and converted to fat) my body fat stays stable no matter how much fat I consume - or calories. I have found it impossible to "overeat" with a high-fat, low-carb lifestyle. The moment I start going higher-carb the body fat % starts to creep up again regardless of how many calories I am consuming. The number on the scale goes up faster because my body will also start retaining too much water since carbs also cause quite a bit of water retention.

My carb addiction is an ongoing battle so I have been watching this happen.

You didn't gain fat because of the excess carbs. You gained it because you either went over your TDEE or you didn't burn as many calories as you thought you did. You gained water weight most likely which passes.

Check out Lyle McDonald here: http://www.bodyrecomposition.com/fat-loss/how-we-get-fat.html

Its all about the 1st law of thermodynamics, you can't break the laws of physics.