Is Sugar High And Crash A Myth?

[davekm]

Here are some things I've found:

 

I wonder if the 8 minute insulin rise has any lasting effects on the body. Also, is it true that you need to eat refined sugary crap to increase serotonin in the brain?

"In a non diabetic individual, blood sugar is closely regulated by at least 2 hormones with opposing actions. Insulin is released by the pancreas when a glucose load is sensed. This, as you have stated lowers the blood sugar levels. Insulin has a life span of approximately 8 minutes in the blood stream, which is really not very long. Should the blood sugar drop too low, the pancreas releases glucagon. The main action of glucagon is to signal the liver to take some of the 400+ Kcals worth of it's stored glucose and release that into the blood stream. This hormone can act with in seconds of its release. In fact, it is so powerful and quick that some diabetics carry it with them to counteract severely low blood sugar reactions.

 

So, I would generally that the idea of a rush followed by a crash in a healthy individual is at least an overstatement and more like a myth."

 

"There's no evidence to support the idea that mid-afternoon tiredness is caused by hypoglycemia, or that healthy people feel normal fluctuations in blood sugar," says Dr. Phillip Cryer of the Washington University School of Medicine."

[CraigD]

Welome to hypography, Dave! :) Please feel free to start a topic in the introductions forum to tell us something about yourself.

I wonder if the 8 minute insulin rise has any lasting effects on the body.

The 8 minute life-span Cryer mentions isn’t for a rise in insulin in the blood and tissues, but about how long, on average, a molecule of insulin released by the pancreas exists before it becomes so damaged (“degraded”) that it can no longer signal a cell to use glucose. In a normal human (and in nearly all other non-microscopic animals), the pancreas releases insulin as needed to regulate the concentration of glucose in the blood fairly precisely – in humans, between about 0.8 and 1.2 grams/litre. So it’s good that insulin is degraded quickly, or it would be hard for the body to regulate blood glucose levels, because the pancreas can only add, not remove, insulin from the bloodstream.

 

Also, is it true that you need to eat refined sugary crap to increase serotonin in the brain?

No.

 

Humans and other animals experienced increases and decreases in the amount of serotonin in the neural synapses in their brains (and other important places in the body, such as the intestines, where serotonin plays an important role in regulating digestion) for many thousands of years before anyone learned how to refine sugar from plants and make sugary crap (also known as yummy treats) out of it.

 

Serotonin is a complicated neurochemical, and a difficult one to directly measure in action, so it’s hard to make definitive statements about it, but we have a pretty good sense that having a lot of it in your brain synapses makes you feel something describable as safe, happy, and content. Such increases appear to occur in response to us experiencing events that produce this feeling, due to using licit and illicit drugs ranging from LSD to Prozac, or for little apparent reason other than that we get this feeling.

 

I agree with Cryer’s opinion that

"There's no evidence to support the idea that mid-afternoon tiredness is caused by hypoglycemia, or that healthy people feel normal fluctuations in blood sugar."

However, given the many ways that brain serotonin levels can be affected, and given our species love of sweet-tasting foods, I don’t think “sugar highs” and “crashes” are complete myths. They are, I think, caused by physiological processes more complicated than digestion alone.

[davekm]

It is the 8 min insulin spike that carries tryptophan to the brain, is it not? I don't know how much an 8 minute insulin spike can increase brain tryptophan though.

 

Does this 8 minute insulin spike cause any other effects, beyond an increase in serotonin? Does this serotonin high precede a serotonin crash?

 

Thanks

[CraigD]

It is the 8 min insulin spike that carries tryptophan to the brain, is it not?

No. Please reread my first post, or another description of insulin metabolism, such as at this wikipedia article.

 

There is no spike in insulin levels, 8 minutes long or otherwise. When the amount of glucose in blood increases, usually due to eating and drinking foods, which are converted into glucose by digestive processes, insulin is secreted into the blood by the pancreas, signaling cells (especially liver cells) to absorb glucose and store it as glycogen. The pancreas continues to secrete insulin until glucose levels are at a mid-range concentration, which, if a lot has been eaten, or eating goes on for a long time, can take hours.

 

Though the primary function of insulin is signaling cells to absorb glucose and convert it into glycogen, it signals many other cellular processes, including absorbing proteins in the blood. Tryptophan is one such protein, one of the 20 or so amino acids from which other proteins, such as serotonin, are synthesized by various metabolic processes. However, insulin doesn’t carry tryptophan or any other protein to the brain, or anywhere. Tryptophan, insulin, and other molecules are carried by the blood to various cells, where they “leak” in a controlled way through the walls of blood vessels into the spaces between cells, then are absorbed, also in a controlled way, by the cells.

 

The brain is a special organ, in that the blood vessels in it allow only small molecules to leak into the space between brain cells. The amino acids, tryptophan included, are small, and can pass this “blood-brain barrier”. Insulin, though it’s a large molecule, can, too, because it’s recognized by the cells lining the blood vessels and “transcytolsed” through.

 

Some molecules, especially drugs and disease pathogens, depend on “hitching a ride” with insulin or other hormones through the BBB, but tryptophan, being small and already allowed through, doesn’t need to.

 

I should correct a mistake I made in my previous reply. I wrote:

So it’s good that insulin is degraded quickly, or it would be hard for the body to regulate blood glucose levels, because the pancreas can only add, not remove, insulin from the bloodstream.

Though the majority of the pancreas is dedicated to producing insulin, it can also produce and release glucagon, a hormone that signals liver cells to convert glycogen to glucose.

 

That’s what I get for thinking I know insulin metabolism well enough to post about it without doing any research – I end up making up stuff that’s just plain wrong! :doh:

[davekm]

So, how do sugary, high GI foods raise serotonin?

Edited May 17, 2012 by davekm

[CraigD]

So, how do sugary, high GI foods raise serotonin?

There’s a lot of serotonin in human and other animal bodies, playing a lot of different roles, so where it occurs at a particular concentration is as or more important than what that concentration is. For now, I’ll guess you mean “raise serotonin concentration in all brain synapses”, because these levels appear to affect mood, so might provide a purely neurophysiological explanation of a “sugar rush”.

 

That said, I’m not sure sugar and other high glycemic index foods actually do, by themselves, significantly affect synaptic serotonin levels. Glucose – what high GI foods convert to more easily than low GI foods – isn’t a biochemical precursor of serotonin (its precursor is tryptophan, which is found mostly in eggs, meat, cheese, seeds and beans) , nor a direct moderator of its synthesis. As I mentioned in my previous post, raising blood glucose raises the uptake of it into cells, including those of the blood brain barrier, a mechanism that creates an opportunity for many molecules that can’t usually pass the BBB to “hitch a ride” past it, but how this would ultimately affect synaptic serotonin, I can’t guess.

 

Whether increases in synaptic serotonin produce a psychological rush is also hard to say with certainty. It’s pretty clear it affects moods such as depression and anxiety, but precisely how it does remains a mystery, especially since elevating its levels doesn’t always appear to reduce depression and anxiety, or lowering it, decrease them.

 

All this is further confused and complicated by the difficulty of actually measuring where serotonin (or practically any other neurotransmitter) is in the brain – whether it’s inside the synapse, actually functioning as a neurotransmitter, or outside it, in the spaces between. At present, the only ways I know of to do it involve either getting fluid or tissue out of the brain, such as with a needle (or a common lab technique commonly called “mind blowing”, which I’ll say no more about in this post other than it involves compressed air and is nasty :eek2:), or, recently, by implanting a miniature devices (ie: the Mayo clinic-based DBS consortium’s WINCS sensor). None of these techniques are very good at distinguishing between serotonin inside vs. outside of synapses.

 

Based on personal observation and science literature, my guess is that the “sugar rush/crash” involves a lot of psychology – that is, that it occurs in large part because our people in our culture expect it to.

 

Our bodies are pretty effective at allowing us to eat all sorts of foods, including sugars, without having much of a psychotropic effect. Our psyches and society, on the other hand, are prone to forming belief and expectations, and validating them with weak anecdotal evidence. Of course, because something has a primarily psychological, rather than a physiological, cause, doesn’t mean it’s not real, but the distinction is a critical one.

 

There’s a good bit of evidence that, just the opposite of causing a rush, high carbohydrate foods (including sugary ones) cause drowsiness. My read of the science and anecdotes, leads me to conclude that sugary foods can cause a mild rush OR drowsiness, depending on circumstances, especially how recently and how much you previously ate.

 

:) Isn’t physiology fun?! I find that many folk believe most of it is known science, practically part of money-making technology, but there’s a huge amount of important knowledge that’s mostly guesswork, much of it likely wrong, just not known, or not even imagined. A person can spend a lifetime studying physiology (and make a lot of $$$ in the process, too).

[davekm]

So, the fact that more amino acids are absorbed into the blood, doesn't mean more make it to the brain? I've read that sugar increases dopamine & epinephrine. Is this true and could this be responsible for the sugar high?

[CraigD]

So, the fact that more amino acids are absorbed into the blood, doesn't mean more make it to the brain?

When there are more amino acids in the blood, more are absorbed by cells, including those in the brain.

 

Amino acids, however, aren’t formed from sugar or other carbohydrates.

 

I've read that sugar increases dopamine & epinephrine. Is this true ...

I believe you have this relationship backwards.

 

Increased epinephrine (AKA adrenaline) is not caused by glucose or other sugars. Epinephrine indirectly increases blood glucose, mainly by causing the pancreas to release glucagon and suppressing its release of insulin, which causes cells, especially the liver, to release glucose.

 

... and could this be responsible for the sugar high?

The point I tried to make in my previous post is that we need to be skeptical of the assumption that “the sugar high”, as it’s commonly believed to, actually occurs. Before considering what causes a thing, it’s important to define precisely and objectively what that thing is, and devise objective ways to measure it.

 

I’m unaware of this having been done with the “sugar high/crash.” Rather, the evidence for it I’ve heard and read consists of anecdotal confirmation, both of the expectation that consuming sugary food and drink makes one “high” and more active, AND that it makes one low and less active. I suspect that both observations are true, or false, depending on the psychological and physiological specifics of different situations.

 

It would be a good science, I think, to track down existing research along these lines – or, if none or too little exists, create some. This would allow a better and more conclusive answer to this thread’s title question, “is [the] sugar high and crash a myth?”

[davekm]

Just found this on another forum. What do you make of it Craig?

 

"There's insulin receptors in the brain, so while you can't directly feel the sugar levels (so far as I know only the pancreas can detect those), but you can definitely feel the insulin."

[cal]

It is the 8 min insulin spike that carries tryptophan to the brain, is it not? I don't know how much an 8 minute insulin spike can increase brain tryptophan though.

 

Does this 8 minute insulin spike cause any other effects, beyond an increase in serotonin? Does this serotonin high precede a serotonin crash?

I realize the physiological science behind this is under debate, as this thread is dealing with so far, but I'd like you to know that sugar spikes (followed by insulin spikes) do for sure have an affect on your brain, there is loads of evidence and experiments showing this, but since it's only a google entry away, I'm assuming you already know that there is an effect. You seem to be asking what the effect really is and if what we attribute to sugar highs is actually caused by sugar intake. One aspect of this that I think you should look at is ADD and ADHD patients that change their diets. If you google nuerofeedback or dietary changes used to combat Attention Deficit Disorder (which is a misnomer btw) you'll find that by cutting out all white-processed sugars, or by significantly limiting all sugar intake (to less than 20-40 grams a day) that the symptoms of ADD (and I think ADHD too) are severely reduced to the point that the afflicted individuals are usually no longer diagnosable for having ADD.

 

That being said, high sugar intake has other affects on your brain beyond an increase in serotonin. Normal people don't feel the effect as much because their brains are more regulated and reach homeostasis quicker, but you can see the effect taking a more drastic role in the brain of an ADD-affected person. That link shows the Delta and Theta wave production in the human brain is significantly more active in a person with ADD, and both those brain waves are stimulated by high sugar intake as well which lead to hyper-activity or hyper-sensitivity of the person (aka Sugar Rush). A sugar rush, or "sugar high" (as far as I can tell, these terms are interchangeable), usually only lasts a few hours in a normal person, but science can see that in a person with ADD, where the sugar unbalances brain activity more, that it affects many things besides the physical feeling of energy from your body; it affects focus and alertness, and by extension mood.

 

I can't think of any other examples where sugar's effect on the brain is exaggerated, so I'm not sure if there's other ways of proving that there is an effect, but I hope this sheds some light on it.

[CraigD]

Just found this on another forum. What do you make of it Craig?

 

"There's insulin receptors in the brain, so while you can't directly feel the sugar levels (so far as I know only the pancreas can detect those), but you can definitely feel the insulin."

I think the observation about insulin receptors in the brain is correct, but the rest, not.

 

For years – including the ones when I took physiology classes – science believed insulin didn’t have much function in brain and other nerve cells, because they’re known to be able to metabolize (“burn”) glucose without insulin signaling specialized protein structures in the cell walls to transport (“pump”) glucose into most cells, such as muscle cells. In just the past 10-5 years or so, however, experiment on nerve cell cultures and in simple animals show that insulin plays a different, possibly very important role, in nerve cells: it appears to play a role in the way nerve cells reconnect themselves, which has a strong but only somewhat understood role in “learning” low level “skills”, such as visual perception. For example, this 2008 ScienceDaily article describes experiments on tadpoles by Chiu, Chen, and Cline, where genetically altering or blocking insulin receptors in tadpoles (juvenile frogs) caused them to have abnormal responses to light, and when examined microscopically, have abnormal nerve structures.

 

Something similar almost surely occurs in human brains, insulin playing an important role in the the formation of our brains and other nervous system structures. However, insulin is not a neurotransmitter, and doesn’t have an immediate strong effect on neural activity, so I don’t think its accurate to say we can “feel” its effect the way we (especially those of us with diabetes) can feel high or low blood glucose levels, or feel psychoactive chemicals, endogenous (produced within the body) or external, such as mind altering drugs, licit or otherwise.

 

Insulin plays a lot of different metabolic roles (see here for a summary) – as recent research like the above shows, we’re still learning about new ones – but its primary role, as we’ve discussed earlier in this thread, is signaling cells, mostly those in the liver, to store glucose as glycogen, removing it from blood.

 

Abnormally high (above 2 g/L) or low (below 0.8) blood glucose levels have dramatic psychological and philological effects – typically torpor and lethargy for high, dread, panic, loss of consciousness and even death for low – but because glucose-managing systems works well in normal, healthy people, such levels occur only in abnormal situations, such as people with diabetes, or when normal people are given injected insulin.

 

Prior to the creation of more effective drugs, large doses of insulin were sometimes give to induce coma to treat severe psychiatric disorders (“insulin shock therapy”), but the efficacy of this treatment was believe to be due to the interruption of abnormal thinking caused by the long, deep unconsciousness of coma, not any neurophysiological action of insulin.

 

As I said in this post last year

... we need to be skeptical of the assumption that “the sugar high”, as it’s commonly believed to, actually occurs.

Restating more strongly: there’s no positive scientific evidence that sugar “highs and crashes”, as they’re commonly described as similar to stimulant drug highs and crashes, actually exist. Studies in which people suspected of responding adversely to eating sugary foods and drinks (eg: children diagnosed with ADHD) in which they are given sugary and sugar-free (placebo) sweets, but neither researcher not subject knows which (the experiment is double-blind), react the same to the either. This strongly suggests that the cause of sugar highs and crashes is psychological, not physiological. (see here for a few links)

 

Answering this thread’s title question “is sugar high and crash a myth?” science strongly suggests the answer is “yes”.

[davekm]

Why then do people crave sweet, sugary foods? I include myself amongst those people. Is this a dopamine/endorphins reaction or just simply because it tastes nice?

 

I know all the evidence points to it being a myth, but I just found this on wikipedia about postprandial somnolence. Is this false?

Insulin stimulates the uptake of valine, leucine, and isoleucine into skeletal muscle, but not uptake of tryptophan. This lowers the ratio of these branched-chain amino acids in the bloodstream relative to tryptophan[4] (an aromatic amino acid), making tryptophan preferentially available to the large neutral amino acid transporter at the blood–brain barrier.[5] Uptake of tryptophan by the brain thus increases. In the brain, tryptophan is converted to serotonin,[6] which is then converted to melatonin. Increased brain serotonin and melatonin levels result in sleepiness

 

Insulin also can cause Postprandial somnolence via another mechanism. Insulin increases the activity of Na/K ATPase, causing increased movement of potassium into cells from the extracellular fluid.[9] The large movement of potassium from the extracellular fluid can lead to a mild hypokalemic state. The effects of hypokalemia can include fatigue, muscle weakness, or paralysis.[10] The severity of the hypokalemic state can be evaluated using Fuller's Criteria.[11] Stage 1 is characterized by no symptoms but mild hypokalemia. Stage 2 is characterized with symptoms and mild hypokalemia. Stage 3 is characterized by only moderate to severe hypokalemia.

Edited April 15, 2013 by davekm