Et Tu Fox? – “bad” Fast Food

So I’ve got Fox running on the TV. The cute talking head and the guy-in-suit-remote reporting on Trump, his medical report, and diet. They indulge in the now far too common “shaming” of Trump’s love of “fast food” and strongly imply (frankly, flat out say) that to lose weight he needs to let go of the “fast food”.

Sigh.

This is just so daft, I don’t know where to begin. I know it is a “push” form the left to put Food Nazis in charge of our diet and get us all to eat a lot less, preferably vegetarian, and never anything from an evil “corporation”… ( I have several family and friends from the vegetarian / vegan side of things); but really, can you just THINK for one moment?

OK, the “approved” meal:

A nice bit of French Bread, a light salad, perhaps with some Thousand Island dressing on it, a side vegetable, and at most 4 ounces of meat. Oh, and the French Bread not buttered…

Now consider the “evil” fast food burger and fries:

First off, the fries ARE a side vegetable. No, not a green one, but potatoes are on the “approved” and “good” list, after all…

Now take your French Bread, and make it shaped into a bun… The typical “condiments” of mayo, catsup, and mustard, with a bit of pickle, if mixed together makes Thousand Island Dressing ( I’ve done it often when needing a quick salad dressing. We did it in the restaurant when we’d run out of the commercial stuff in gallons…) Your lettuce, tomato, onion, etc. is a light salad. Put them on the bread / bun. Now add the “6 to a pound” patty, or 2.6 ounces of beef.

What you have in front of you is EXACTLY the same in terms of calories and diet as the “approved” meal, though 1.4 ounces “better” on the low meat side…

The “approved” meal:

A nice pasta with Marinara sauce including mushrooms, olives, and salami, topped with cheese.

The “evil” fast food:

A wafer of bread (same amount of wheat as the pasta) topped with Marinara, salami, mushrooms, olives and topped with cheese. Roasted. That is, the “evil” fast food Pizza.

Same ingredients, same calories. Slightly different processing.

The “approved” meal:

a 3 ounce fish patty, a small side salad with dressing, a medium dinner roll.

The “evil” fast food:

a 3 ounce fish patty, on a medium bun, along with a small salad topped with dressing. AKA “Fish Sandwich” from your fast food place.

The “approved” meal:

At home, you have a fresh salad made with cabbage, carrots, etc. and a touch of buttermilk dressing, a serving of baked beans, and 6 ounces of roasted chicken.

The “evil” meal:

Order up a 2 or 3 piece (size varies a bit by location) chicken meal at KFC with a side of slaw and baked beans. You can get it roast / skinless IIRC, or fried.

The “evil” meal:

Taco Bell. (This one is so blatant I can’t even find a way to hide it…)

The “approved” meal:

The very same burrito, taco, taco salad, “whatever” made at home or ordered in a fancier Mexican Place. Look, it’s a flour or corn tortilla along with some combo of refried beans, Spanish rice, salad, cheese, and salsa, with optional “meat stuff”. All in various combinations and permutations. Just Like Taco Bell.

Now there might be some difference in the particulars of the tortilla or refritos, but I’d guess both of them come from a factory somewhere in either case. When cooking at home, I use canned refried beans as they are as good as I could make, vegetarian available – i.e. no lard, and very convenient. I also used packages shredded cheese just like the “pros” and tortillas from a major commercial maker, just like everyone else. At “higher end” places like Chipotle Mexican Grill, you get more choices of bean color and smashed or not smashed, but that isn’t going to change how healthy it all is.

In Conclusion

I could go right on down the list of ethnicities, but why bother. You get the picture. When I travel, I typically hit Jack-In-The-Box for their Breakfast Jack. It is a bun (bread) with a fried egg, slice of sandwich ham, slice of cheese, and nothing else I’ve noticed. Essentially identical to a small ham and cheese omelette with toast. Now how is my health improved by ordering a ham and cheese omelette with toast at $10 / plate instead of 2 BFJacks at about $3? Not at all. (Oh, and both can be ordered with hash brown potatoes).

So please please please, can folks start giving some “push back” on the “Fast Food Evil And Fattening” meme? It isn’t the shape of the food (typically sandwich) nor the ingredients (substantially the same) that’s the issue. It’s how much of it you stuff down the gullet and if you wash it down with a 1/2 gallon of Fructose Syrup pretending to be a soda. (Fructose is directly metabolized to fat in the liver…) At “fast food” places, I typically order a bottle of water or get UN-sweetened iced tea (no fructose) and add my own sugar (sucrose) in moderation.

Does nobody bother to look at what ingredients are used to assemble their meals and notice they are the same things? Maybe it was growing up in a restaurant and having a very early introduction to “how to make 100+ different meals from 10 different ingredients”…

Somehow I thought Fox News would know better… I expect that kind of stupid from MSNBC, as they have bought into the Left POV Food Shaming thing…

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About E.M.Smith

A technical managerial sort interested in things from Stonehenge to computer science. My present "hot buttons' are the mythology of Climate Change and ancient metrology; but things change...
This entry was posted in Food, Political Current Events and tagged , , , . Bookmark the permalink.

17 Responses to Et Tu Fox? – “bad” Fast Food

  1. Svend Ferdinandsen says:

    It’s how much of it you stuff down the gullet!”
    You are so right. It is amazing how most advises goes on to eat more of what they call helthy products, when in fact the best advise would be to eat less of whatever you eat.

  2. philjourdan says:

    My diet has changed with my age. Due to necessity (I do not want to balloon up to 300 pounds). But I do not eat “healthy”. Ewell Gibbons did, and it did not do him much good.

    I am always reminded of the cartoon of the old guy on the doctor’s table, hunched over, and his doctor saying “You know those extra 20 years I promised you if you ate healthy? These are them.”

    I may not live to be 100. But I will enjoy the time I do live.

  3. Larry Ledwick says:

    (Fructose is directly metabolized to fat in the liver…)

    That assertion has always bothered me.
    Sucrose is composed of Fructose and glucose molecules “stuck together” the first step in metabolizing sucrose is cleaving those two simple sugars so about 50% of your sucrose intake is immediately converted to fructose. From there it is processed in the liver but among the things that can happen to it, is the liver can convert fructose to glucose (about 35%) or Lactate (about 28%) — so about 65% of your fructose intake gets converted to those more useful sugars by the liver. Some of it does get converted to triglycerides (fat in the blood stream), but about 70% of our energy consumed in light fully aerobic exercise is from fat metabolism that is not a problem. We need fats in the blood stream.

    https://nutritionandmetabolism.biomedcentral.com/articles/10.1186/1743-7075-9-89

    If the concerns about fructose was true, I would be a blimp, as I practically live on soda pop as something close to 50% of my caloric intake is from soda pop. (before everyone screams — I do take vitamin supplements.) My weight / BMI is typical for my age and build within the normal range for my age.

    The difference is I am a light eater. I gain weight if I eat over 1500 calories a day, my normal intake is between 1200 – 1700 calories a day. (I recently kept a food diary for a month to quantify my intake).

    I am a grazer, and do not eat huge meals but snack almost constantly all day long.
    Typical intake would be 2 eggs with a glass of milk for breakfast
    1/2 of a cinnamon roll for lunch, and 2 simple sandwiches for dinner with a glass of milk.
    All the rest of my food intake would be 4 -5 servings of soda pop totaling about 60 oz.
    I have been eating this way for about 40-50 years.

    If I am really feeling healthy I will have a glass of V8 juice in the morning, or a bowl of vegetable soup for dinner, sometimes a 3-4 ounce salad with a small serving of spaghetti for dinner.
    I can’t even finish a large hamburger like a Whopper and fries, I will leave 1/3 of it uneaten. If I go to a restaurant and get some BBQ beef or something I “doggy bag” it home and get 3 meals out of it.

    The only thing that matters is calories in vs calories out. Your body will figure out how to use what you give it as long as it includes a few must have trace minerals, vitamins and essential proteins.

  4. H.R. says:

    Loved the ingredient comparison, E.M.

    It seems that “Fast Food” is now two 4-letter words.

  5. M Simon says:

    We have had “substance Nazis” for quite some time. They usually come from the left. But these days the right is joining in. As they did in the 1932 election.

    The beginning of these campaigns is to make the substance a moral issue.

  6. p.g.sharrow says:

    I have always considered a well made hamburger to be real, quality food.
    Now sugared water is another thing. The only drink that is less desirable is those made with sugar substitutes. We are fortunate to have very good drinking water from a well sealed deep well.
    Fries cooked in tallow and lard were wonderful but, modern ones are boiled in Canola oil, yuck! (rape seed oil), toxic stuff that ruins the flavor and causes digestive problems for some of us.
    Pizza is wonderful as long as the institutional tomato past is not used. Gives me terrible heartburn. Homemade no problem. I think it is the corn derived sugar that is the cause. Not all sugars are made the same. Different constructed molecules are broken down in different manners that create other side effects…pg

  7. E.M.Smith says:

    @Larry:

    I was launching into a nice tirade about how fructose is metabolized, based on what I remembered of some semi-tech article a year or two back, that claimed roughly what I was about to spout, and then decided to find a reference. I like references, the more technical the better.

    Well, a few puff pieces later, I found a Very Nice and Very Technical article that included examples of the use of alcohol dehydrogenase and that fructose will pressure that pathway as much as alcohol does and … and then the damn thing went into even MORE detail than the prior article… which, it seems, had “abbreviated for the public” a bit too much. I hate that…

    So now all my loverly tirade in the making has to get a strikeout…


    It is excess fructose that gets the conversion. Yes, sucrose is 1/2 fructose, so right off the bat, you are 50% ahead… the glucose is directly metabolized in the body cells.

    Most folks in the USA don’t eat light, like you do, so they store the fructose… as fat. Given your low calorie intake, anything you consume is going to be pounced on for immediate fuel. The problem is for “the rest of us” who have extra calories, in a big bolus, in a point in time meal. Flooded with food, the body starts storing it away. Glucose to glycogen (starch to glucose), and fructose to fatty acids in the only place it is metabolized, the liver. That then joins the fats from the meal in their rush though the blood to the fat cells for storage.

    Now if calorie lite, and ‘grazing’, you have a constant demand for fuel, and steady supply. The soda just flows in with the rest and the liver turns it into what’s needed now, to the extent it can.

    No, the real reason Fructose is bad seems to be a bit different:

    http://themedicalbiochemistrypage.org/fructose.php

    doesn’t want me to cut / paste a comment, so I can either snapshot the whole page or just put a pointer here. … he wonders how annoyed that makes him… saves the whole damn page as text and pastes way too much here in spite…

    The key bit is down on the second or third page. It points out that the particular way fructose and glucose are metabolized in the brain result in glucose causing ‘I am full’ feedback and fructose causing ‘I am hungry’ feedback. They go out of their way to point out High Fructose Corn Syrup is only 55% Fructose (and sucrose is 1/2) but that would still shift the hungry / not-hungry balance of the feedback to the ‘;i am hungry’ side. I’ve bolded it:

    BEGIN QUOTED TEXT:

    Diets containing large amounts of sucrose (a disaccharide of glucose and
    fructose) can utilize the fructose as a major source of energy. It
    should be pointed out that the difference between the amount of fructose
    available from sucrose obtained from cane or beet sugars is not
    significantly less than that from corn syrup. Corn syrup is somewhat
    improperly identified as high fructose corn syrup (HFCS) giving the
    impression that it contains a large amount of fructose. However, whereas
    the fructose content of sucrose is 50% (since it is a pure disaccharide
    of only glucose and fructose), the content in HFCS is only 55%. The
    reason HFCS has more than 50% fructose is because the glucose extracted
    from corn starch is enzymatically treated to convert some of the glucose
    to fructose. This is done in order to make the sugar sweeter which is
    why it is particularly popular in the food industry. Therefore, any
    disorder and/or dysfunction (see below), attributed to the consumption
    of fructose, can be manifest whether one consumes cane or beet sugar or
    HFCS.

    The pathway to utilization of fructose differs in muscle and liver due
    to the differential distribution of fructose phosphorylating enzymes.
    Hexokinases are a family of enzymes that phosphorylate hexose sugars
    such as glucose. Four mammalian isozymes of hexokinase are known (Types
    I–IV), with the Type IV isozyme often referred to as glucokinase.
    Glucokinase is the form of the enzyme found in hepatocytes and
    pancreatic β-cells. Several of the hexokinases (but not type IV) can
    phosphorylate various different hexoses including fructose. In addition
    to hexokinases, fructose can be phosphorylated by fructokinases.
    Fructokinases are formally referred to as ketohexokinases (KHK). There
    are two forms of KHK in mammals that result from alternative splicing of
    the KHK gene. These two isoforms are called KHK-A (fructokinase A) and
    KHK-C (fructokinase C). Fructokinase C (KHK-C) has a very high affinity
    for fructose resulting in rapid phosphorylation with concomitant
    depletion in ATP. Fructokinase A (KHK-A) has very low affinity for
    fructose thus, exerting minimal effects on overall fructose metabolism
    and levels of ATP. Expression of fructokinase C (KHK-C) is seen
    primarily in the liver, pancreas, kidney, and intestines. Expression of
    fructokinase A (KHK-A) is more ubiquitous and expressed at highest
    levels in skeletal muscle. Although both fructokinase C (KHK-C) and
    fructokinase A (KHK-A) can metabolize fructose, fructokinase C (KHK-C)
    is considered to be the primary enzyme involved in fructose metabolism
    because its’ K_M for fructose is very much lower than that of the
    fructokinase A (KHK-A) isoform. Because of its very high K_M for
    fructose there is some question as to whether or not fructokinase A
    (KHK-A) actively metabolizes fructose /in vivo/.

    Muscle, which contains two types of hexokinase (type I and type II), can
    phosphorylate fructose to F6P which is a direct glycolytic intermediate.
    However, the affinity of hexokinase for fructose is substantially less
    than that of fructokinase.

    The liver expresses predominantly glucokinase (hexokinase type IV) which
    is specific for glucose as its’ substrate. Due to this pattern of
    expression there is the requirement for KHK in order to deliver fructose
    into hepatic glycolysis. Hepatic KHK-C phosphorylates fructose on C–1
    yielding fructose-1-phosphate (F1P) which is then hydrolyzed by a
    specific isoform of aldolase.

    Humans express three distinct forms of aldolase; aldolase A, aldolase B,
    and aldolase C. Aldolase A (fructose-1,6-bisphosphate aldolase) is
    expressed in most tissues. Aldolase A catalyses the hydrolysis of F1,6BP
    into two 3-carbon products: dihydroxyacetone phosphate (DHAP) and
    glyceraldehyde 3-phosphate (G3P). The aldolase A reaction proceeds
    readily in the reverse direction, being utilized for both glycolysis and
    gluconeogenesis. The aldolase A gene (gene symbol: ALDOA) is located on
    chromosome 16p11.2 spanning 7.5 kb and is composed of 12 exons that
    encode a 363 amino acid protein. Aldolase B is expressed primarily in
    the liver but also to some degree in the kidney and small intestine.
    Aldolase B is unique from the other two isoforms in that it can catalyze
    the hydrolysis of both fructose-1,6-bisphosphate and
    fructose-1-phosphate with equal affinity. The aldolase B enzyme is
    encoded by the ALDOB gene which is located on chromosome 9q21.3–q22.2
    and is composed of 9 exons that produce a protein of 363 amino acids.
    Aldolase C is expressed in the brain. The aldolase C enzyme is encoded
    by the ALDOC gene which is located on chromosome 17cen–q12 and is
    composed of 10 exons that produce a protein of 364 amino acids.

    In the liver, aldolase B can utilize both F-1,6-BP and F1P as
    substrates. Therefore, when presented with F1P the enzyme generates DHAP
    and glyceraldehyde. The DHAP is converted, by triose phosphate isomerase
    (TPI), to G3P and enters glycolysis. The glyceraldehyde can be
    phosphorylated to G3P by glyceraldehyde kinase or converted to DHAP
    through the concerted actions of alcohol dehydrogenase, glycerol kinase
    and glycerol phosphate dehydrogenase.

    Reactions of fructose metabolism

    Entry of fructose carbon atoms into the glycolytic pathway in
    hepatocytes, kidney, and small intestine.


    Fructose Effects on Food Intake

    As pointed out in the Glycolysis
    page, glucose is
    the primary fuel used for energy production in the brain. When glucose
    is metabolized within the hypothalamus, a signaling pathway is initiated
    that ultimately results in the suppression of food intake. More detailed
    information on the role of the hypothalamus in the control of food
    intake can be found in the Gut-Brain Interrelationships
    page. The
    principal participants in this signaling cascade include AMPK
    , acetyl-CoA carboxylase
    (ACC), and the product of the ACC reaction, malonyl-CoA. The mechanism
    by which AMPK and ACC are regulated, ultimately resulting in altered
    levels of malonyl-CoA are detailed in the Lipid Synthesis
    page.
    Briefly, activation of AMPK results in the phosphorylation of ACC
    resulting in reduced activity of the latter enzyme. Conversely, when
    AMPK activty falls the phosphorylation state of ACC falls resulting in
    increased production of malonyl-CoA. When glucose oxidation is increased
    in the hypothalamus there is a resultant dephosphorylation and
    inactivation of AMPK and thereby, activation of ACC. The resultant rise
    in hypothalamic malonyl-CoA is correlated to reduced expression of
    several orexigenic peptides (e.g. ghrelin, NPY, and AgRP) concomitant
    with activated expression of several anorexigenic peptides (e.g. α-MSH
    and CART). These changes in neuropeptide expression result in suppressed
    food intake while simultaneously increasing overall energy expenditure.

    In contrast to the anorexigenic effect of hypothalamic glucose
    metabolism, the metabolism of fructose in the brain exerts an orexigenic
    effect. Although the overall mechanisms by which fructose exerts this
    orexigenic effect are complex, it is due, in part, to the fact that the
    brain, like the liver, possesses a unique set of sugar transporters and
    metabolizing enzymes that enables fructose to bypass the PFK-1 catalyzed
    step of glycolysis. The PFK-1 catalyzed reaction is the rate-limiting
    step in glycolysis and is critical in the overall regulation of ATP
    production and consumption. Since hypothalamic fructose metabolism
    bypasses this important regulatory step its metabolism rapidly depletes
    ATP in the hypothalamus. When ATP levels fall there is a concomitant
    rise in AMP which results in activation of AMPK. Activation of AMPK
    results in phosphorylation and inhibition of ACC which then results in
    decreased malonyl-CoA levels in the hypothalamus. Therefore, although
    glucose and fructose utilize the same signaling pathway to control food
    intake they act in an inverse manner and have reciprocal effects on the
    level of hypothalamic malonyl-CoA.

    Numerous experiments in animals have implicated malonyl-CoA as a key
    intermediate in the regulation of feeding behavior and overall energy
    balance initiated via signaling cascades within the hypothalamus.
    Initial evidence demonstrating this role of malonyl-CoA was the finding
    that inhibition of fatty acid synthase (FAS) suppressed food intake. FAS
    is the primary enzyme in the /de novo/ biosynthesis of fatty acids
    . The fungal
    antibiotic, cerulenin, and a related analogue C75, bind to the active
    site of FAS thereby inhibiting its activity. When these compounds are
    administered to mice there is a resultant decrease in food intake. Given
    that inhibition of FAS would be expected to result in an accumulation of
    its substrate, malonyl-CoA, it was suspected that malonyl-CoA may be a
    participant in the observed effects. Indeed, intra-cerebrovascular (icv)
    injection of C75 results in increased levels of hypothalamic
    malonyl-CoA. Importantly, this effect can be reversed by inhibitors of
    ACC, the enzyme which synthesizes malonyl-CoA from acetyl- CoA. Further
    research demonstrated that the anorexigenic effects of FAS inhibitors
    was due to their ability to rapidly suppress hypothalamic expression of
    NPY and AgRP, two key orexigenic peptides, while increasing the
    expression of α-MSH and CART, two key anorexigenic peptides.

    Malonyl-CoA levels in the hypothalamus correlate well with nutritional
    state. Fatty acid synthesis in other tissues, such as the liver and
    adipose tissue, occurs primarily during energy surplus.
    Malonyl-CoA,
    regulates energy metabolism in the liver through two opposing
    mechanisms. It serves as the substrate for FAS during /de novo/ fatty
    acid synthesis while at the same time inhibiting mitochondrial fatty
    acid oxidation through its’ action as an allosteric inhibitor of
    carnitine palmitoyltransferase 1 (CPT1). Inhibition of CPT1 by
    malonyl-CoA prevents entry of fatty acids into the mitochondria, thereby
    inhibiting oxidation. During periods when energy expenditure exceeds
    intake, such as during fasting, malonyl-CoA levels in the hypothalamus
    are low. Following food intake there is a rapid rise in hypothalamic
    malonyl-CoA levels. The changes in hypothalamic malonyl-CoA levels are
    followed quickly by changes in expression of orexigenic and anorexigenic
    peptides. In the fasting state NPY and AgRP levels are high, whereas
    α-MSH and CART levels are low. Upon re-feeding this pattern immediately
    inverts.

    Genetic manipulation of hypothalamic malonyl-CoA levels has also been
    informative. For example, disruption of FAS gene expression in the
    hypothalamus results in increased malonyl-CoA levels and decreases in
    body weight and fat content. Concomitant with disruption of hypothalamic
    FAS gene expression is an increase in malonyl-CoA concentration.
    Additionally, the levels of orexigenic peptides decrease while levels of
    anorexigenic peptides increase leading to suppression of food intake.
    Conversely, genetic manipulation of the expression of malonyl-CoA
    decarboxylase (MCD) has the opposite effects to those seen by disruption
    of FAS expression. MCD functions in opposition to ACC in that it is
    responsible for the conversion of malonyl-CoA to acetyl-CoA. In fact ACC
    and MCD are reciprocally regulated to ensure adequate regulation of
    fatty acid synthesis and fatty acid oxidation. Overexpression of MCD
    within the hypothalamus results in increases in both food intake and
    body weight and also marked increases in body fat content (adiposity).
    Additionally, when MCD expression is increased within the hypothalamus
    there is an observed inhibition of the FAS inhibitor (C75)-induced
    suppression of food intake. These results obtained with forced
    expression of MCD provide strong evidence that hypothalamic malonyl-CoA
    acts as an indicator of energy status and participates in the regulation
    of feeding behavior. In addition, these results indicate that
    malonyl-CoA, rather than fatty acids, is the effector that regulates
    energy homeostasis.

    END QUOTED TEXT.

    So it’s the signaling system that says “eat more and store it as fat” rather than the direct enzymes available per cell tissue type.

    Since you have regulated intake, that doesn’t get a chance to cause you issues, while the ‘fat kid’ with 2 whoppers and a supersized fries gets a big bolus of fructose driven brain regulation saying “Eat it all and I’ll store it as fat”… while the sucrose based drink has a rate limiting step on the bolus of fructose as the sucrose has to be broken down first.

    Well, all I can say for myself is that I had the end state right, even if the exact mechanism was more ‘fuzzy’ in the shorter articles…

    Oh, and really do wish folks who put those “copy is disabled” functions in web pages would realize it just pisses folks off and they “save as text” then cut /paste a whole lot more… since they had to do the extra work…

  8. Larry Ledwick says:

    Good find!
    You point out that there are a lot of secondary factors, I can buy the hunger trigger, as I see that myself in my consumption, if I break the cycle by going to water only for an hour or two the hunger trigger goes away.
    Various factors like natural appetite levels, (which in my case works to my advantage) social pressures to eat fast, social pressures to eat everything on your plate, not having what you really want available in the junk food machine all play a factor. I would be perfectly happy if the junk food machine had things like small rolls and similar bread products but the only thing in there is things like fritos, candy bars, and sometimes cinnamon rolls, all the rest is candy bars I hate, or extra spicy cardboard chips. It is the unqualified dogma that I oppose as you say moderation in all things. Of course when I was running marathons I would chow down on plates of spaghetti and plates heaping with rice covered with a sweet and sour sauce washed down with a coke and I still lost weight (got down to 115 pounds when I was doing it at 5′ 5″)

    I just get bothered by all the food fad nonsense, (eggs are bad — oh wait it is just the yokes — oh wait lots of people don’t have high enough iron intake, whole eggs are a good source, but cholesterol is bad — oh wait it is just the HDL that is bad — oh wait dietary intake of cholesterol has almost zero correlation with blood levels, it is exercise and other factors that determines HDL/LDL ratios — Butter is bad, — Oh wait it is margarine with trans fat that is bad, butter is good — Oh wait refined sugar is a potent drug avoid it at all cost, Oh wait its fructose that is bad but sucrose is good — eat healthy things like raw honey and raisins — Oh wait both have significant fructose)

    Reminds me of global warming almost every single study on foods that claims it is bad ends up getting tossed out 20 years later as bad science — often exactly 180 degrees out.

  9. PaulID says:

    E.M so if i read this right the people you quoted above would tell us to stop eating honey since there is 8% more Fructose in honey than Glucose depending on the honey the total Fructose is as high as 41% while glucose maxes out at 35% also if fructose is that bad why have we evolved to crave it? we are told that eating lots of fruit is good but the sugar we get there is nearly extremely rich in Fructose, which is it? Is it just bad in corn syrup and ok in all other applications or is it not good anywhere or just fine? it can’t be all three.

  10. gallopingcamel says:

    Twenty years ago I ate what I liked and that was plenty of red meat and fried potatoes (I did that to honour the excellent Dan Quayle).

    Then Arthritis locked up my major joints and I learned to live on oily fish. Fortunately I like herrings, sardines, mackerel, trout, salmon etc.

  11. John F. Hultquist says:

    When I was young the neighborhood kids did many types of physical activities. A very few involved organized things, most did not. Kick the can, vacant lot baseball, touch or tackle football, clamp-on roller skates, ice skating, swimming (not in a city pool), badminton, and the list goes on. Now I only see kids doing organized sports that for most involve a lot of standing around or sitting on benches.
    When and if you slow down your food intake better drop. I like to eat, so can’t slow down. Young folks today do not know what it means to be active.

    My father thought pizza was strange and yet liked all the normal ingredients. Maybe that’s why I thought grownups were odd.

  12. E.M.Smith says:

    @PaulID:

    My “thesis” is that fructose, being from fruit in nature, signals to “eat while the eating is good’ in a wild population (i.e. when stuff is ripe and harvest season is here) to pack away some pounds for winter…

    But we’ve made it perpetual harvest season and winter / spring never comes, so we are always putting away the pounds….

    In a normal world, we would get about 1/10 to 1/100 the current sugar intake. Honey is a rare treat and not a significant source of sugars… in the wild…

    In winter, with no source of sugar around, a wild type population would have stored starches and animals to eat. Very little sugar stuff. So fat catabolism would be advantageous and the lack of a ‘store it’ signal a good thing.

    IMHO, things like the Atkin’s Diet take advantage of that asymmetry in sugar signalling.

    For me, I tend to eat fairly little sugar in any case. A tsp or two in tea is about it. The spouse loves sweet stuff and bakes loads of cookies and such. It takes me 2 weeks to get through what she eats in 2 days. OTOH, I’m a grease burner… I’ll eat more fats in a day than she wants in a week. But then I’m full and don’t eat for a long time… That whole hunger signalling system thing.

  13. Gail Combs says:

    “My “thesis” is that fructose, being from fruit in nature, signals to “eat while the eating is good’ in a wild population (i.e. when stuff is ripe and harvest season is here) to pack away some pounds for winter…”
    ……..

    That is my thinking too. For horses grain is going to signal the end of the season so store up fat NOW! Especially for the easy keepers like Shetlands. I have a couple who get pudgy on an 1/8 of a cup -1 heaping Tablespoon of 12% AllStock and that is on grass hay or poor unfertilized pasture.

    I think the obesity problem in the USA is threefold.

    1. Kids with out enough exercise and too much bribing to get good behavior.

    2. Too much substitute of sweet drinks for water and milk. (Soda? What soda. We got soda as a treat on holidays otherwise milk or water with 4 oz of OJ at breakfast.) Now you see kids with a soda bottle permanently stuck to their hand.

    3. Not enough of the right kinds of fats. Fat will turn off your appetite and keep you sated for a long time.

    For us older folks, PILLS, especially the pain killers will make you feel hungry when you are not. Now I find antihistamine also wipes out my stomach and leaves me ‘hungry’ for days.

    OH, and I forgot about salt. The salt on those fries or potato chips will make you thirsty and so the kids drink that much more soda. Soda is where the money is made. This is the whole idea behind the ‘free lunch’ beer nuts.

    Try a restricted salt diet for a couple of weeks (read all labels) to get a feel for just how much our systems are over loaded with NaCl. The food we eat that is ‘lo-fat’ is loaded with sugar to make it palatable too.

  14. Gail Combs says:

    People forget that a lot of Donald Trump’s bulk is a bullet proof vest and not him.

  15. bruce says:

    I tend to match expended energy to intake. No effort = less intake.Thinking doesn’t count as effort.

  16. John F. Hultquist says:

    … with no source of sugar around, a wild type population …

    The Anglo-Saxons might fall into this category.
    Honey was about the only sweet substance available and not a lot of that.
    One of the possibilities of storing calories was wine (alcohol distillation and consumption began mainstream in the mid-1400s). Wine grapes were not a good crop in England so wine was imported. The history of this is a very long tale.
    A place to start: https://en.wikipedia.org/wiki/English_wine_cask_units

    Larger volumes spoil more slowly.
    Too large and casks are not moveable.
    Too small and they go home with the workers.
    The “hogshead” (¼ tun) seems to have been the compromise solution.

    This very long tale explains why “The Master of Wine” qualification is issued from London and not Bordeaux.

  17. E.M.Smith says:

    @Gail:

    I think you have it right.

    @Bruce:

    About 1/4 of heat loss is from the head and the calories consumed by the brain is about the same (at rest), so I think thinking is ‘effort’… but maybe it’s only effort for me :-)

    Unfortunately, the degree of fuel burned doesn’t seem to vary with my thinking about exercise…

    @John F.:

    I didn’t know that… thanks!

    Alcohol directly enters the Citric Acid / Krebs Cycle, so a very efficient fuel.

    Curiously interesting to note that the U.S. gallon started as an English Wine Gallon…

    Makes me like it all the more…

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