Are Fats Unhealthy? The Battle Over Dietary Guidelines
nytimes.com
nytimes.com
>>"We know much less for sure than we think, and recommendations that forcefully tell people exactly what and precisely how much they should or should not eat can be counterproductive."
Unless you have a very acute and well defined health issue like diabetes or severe allergy, people who try to sell you on diet-absolutes are full of nonsense or trying to sell a product.
We need to do more research and learn more before demonizing things like fatty foods. That's all. Not sure what part of this you object to...
CF is a genetic disorder. With CF, your immune system does not work right and you are basically chronically infected with some infection or other. I have a relatively mild form of it, which helped create a situation where I was diagnosed late in life. I finally got diagnosed due to my health deteriorating drastically and I spent a year at death's door. With finally getting a diagnosis, I was empowered to get myself a great deal healthier.
I have fewer blood sugar issues than I used to have. I did nothing to specifically address that issue. I was primarily trying to erradicate the antibiotic resistant infections that were threatening to kill me.
People with CF misprocess fats and most of them are seriously underweight. To my mind, this suggests that fat is probably not the real culprit with diabetes.
I have become very picky about the types of fats I eat. Butter and coconut oil are fats that are very beneficial to my condition. I sometimes get pain under control by spreading a half a stick of butter on a roll and eating that (or did so at one time -- it has been a while as my condition is more stable). Butter and coconut oil are high in saturated fats. My blood sugar is a great deal more stable than it used to be.
(Yes, I know that is "anecdotal." If you want to dismiss it, please come up with a stronger criticism than that. Thanks.)
That said, no one's come up with any vaguely useful citations linking saturated fats to diabetes, and this doesn't help the case for that.
Thank you.
I would be happy to discuss it with you further.
I do not know what you mean by CF is a regulatory derangement.
It is caused by a defect in a specific cell channel that manages traffic of specific molecules into and out of the cell. I have paid enormous attention to that and kind of ignored the hand-wavy and apparently incorrect mental models popular in the medical literature. For example, the official explanation on the CF Foundation website is that people with CF are drowning in an excess of mucus. I found one study that says we produce too little mucus, not too much. This fits with my firsthand experience, it more logically fits with the fact that mucus is a protective coating that helps keep out germs and it fits with the extremely well known and well established fact that women with CF suffer vaginal dryness that often seriously interferes with their sex lives. I think we cough up phlegm, not mucus -- ie infection -- and if you improve mucus production, you reduce infection and see less phlegm. I have seen that hypothesis work effectively for me and my oldest son who has the same diagnosis I have. I have explained it to one woman with CF who was out of time and dying and tracked me down after I left all CF lists and took down my health site. She is gradually getting healthier.
So that is a very long way of saying that a) I have no idea what you mean by that phrase and b) the odds are high that you and I have completely different mental models for what is going on with CF.
It is caused by a defect in a specific cell channel that manages traffic of specific molecules into and out of the cell.
Per Wikipedia: "It is caused by the presence of mutations in both copies of the gene for the protein cystic fibrosis transmembrane conductance regulator (CFTR)."
Per the article on CFTR:
Cystic fibrosis transmembrane conductance regulator (CFTR) is a membrane protein and chloride channel in vertebrates that is encoded by the CFTR gene.
CFTR is an ABC transporter-class ion channel that codes for a protein that conducts chloride and thiocyanate ions across epithelial cell membranes.
More detail:
CFTR functions as an ATP-gated anion channel, increasing the conductance for certain anions (e.g. Cl−) to flow down their electrochemical gradient. ATP-driven conformational changes in CFTR open and close a gate to allow transmembrane flow of anions down their electrochemical gradient. This in contrast to other ABC proteins, in which ATP-driven conformational changes fuel uphill substrate transport across cellular membranes. Essentially, CFTR is an ion channel that evolved as a 'broken' ABC transporter that leaks when in open conformation.
The CFTR is found in the epithelial cells of many organs including the lung, liver, pancreas, digestive tract, reproductive tract, and skin. Normally, the protein moves chloride and thiocyanate ions (with a negative charge) out of an epithelial cell to the covering mucus. Positively charged sodium ions follow passively, increasing the total electrolyte concentration in the mucus, resulting in the movement of water out of cell by osmosis.
So, based on ATP getting to it, it allows movement (passive transport) of a set of ions and H2O in and out of cells. I assume there's some regulatory function that mediates the opening and closing of it; the CF mutations interfere with its function one way or another (e.g. one class is thought to result in the CFTR degrading quickly, don't know if it functions normally while in place).
So while we're mostly focused on the consequences of these ions and water not getting out of the cell and deranging the production of proper mucus, it could also result in metabolic derangement inside these cells. Per https://www.cff.org/Living-with-CF/Cystic-Fibrosis-Related-D... there's a Type 1 style due to direct pancreas damage interfering with production of insulin, but also a Type 2 style interfering with insulin response.
The latter is the sort of thing I'm getting at, I'd want to understand how it works before extrapolating from CF populations to the general one. As the article says, "Unlike people with type 1 or type 2 diabetes, people with CFRD need the same high-calorie CF diet they would normally eat in order to gain weight and build muscle. A healthy diet means eating a variety of foods that are high in protein, fat and salt. The only difference is that people with CFRD need to track or count the foods that affect their blood sugar levels the most." So your eating plenty of fat without apparent harm might or might not be significant for the general population and "normal" Type 2 Diabetes (and I don't know if there's only one form/cause of it).
Still, I am at a serious disadvantage in trying to talk about ion channels and what not in terms that a biologist would typically use.
I did not know this:
Essentially, CFTR is an ion channel that evolved as a 'broken' ABC transporter that leaks when in open conformation.
That is interesting to me. CF is basically a salt-wasting condition. There are various forms of defect in the CFTR, but knowing that it basically leaks may explain why it is basically a salt wasting condition.
(e.g. one class is thought to result in the CFTR degrading quickly, don't know if it functions normally while in place).
If you are interested, I can share my research notes where I spent some time digging up information. I was taking a particular supplement at the time and if I missed a single dose, I drastically and promptly deteriorated. So I was looking to understand why that might be. In the process of digging around, I found that most genetic disorders boil down to being a defect in a particular protein. The CFTR channel is a protein that gets folded a particular way and inserted into the cell membrane in order to handle trafficking into and out of the cell of specific ions.
So one of the things I found was that there are two conditions that cause higher misfolds of proteins within the cell: Derangement of PH level and derangement of salt level. You see both of these things happening with CF.
It is well established that people with CF gradually become increasingly too acid. This is almost never treated. It is not treated as medically significant, even though if you have diabetes and get sudden onset acidosis, they hospitalize you promptly because you can be dead within 72 hours if they can't reverse it. So they know acidosis is deadly. They know CF is deadly. They know CF promotes gradual onset acidosis. No one sees this as related. I decided it must be related and reversing the acidity of my tissues was a cornerstone of my approach.
Initially, I took about $300/month worth of supplements. I thought I would always need to do that. It was a daily battle to try to keep symptoms under control. I gradually became less symptomatic. I stabilized.
So I have concluded that there is a vicious positive feedback loop where the more acid you get, the more you see protein misfolds and the more you see protein misfolds, the more acid you get. I believe this is why it is a degenerative, progressive condition. And if you can accommodate the defect in the cell membrane, which is both a bottleneck on some things and an open flood gate on others at the same time, if you can find a way around that, you can stop and reverse the process.
Presumably this will work differently depending on the specific defect in the CFTR. There are variations of CF that are the equivalent of albinism in terms of simply not producing a CFTR channel to begin with. I imagine that will be much more resistant to management via the process I use.
There are a lot of other things in the back of my mind that are relevant to this discussion, but I am somewhat pressed for time and I am not sure I could make clear what the relevance is.
I do not "eat plenty of fat without apparent harm." I got very picky about WHAT I eat and I believe the high levels of specific things that I ate for a time amounts to redressing a serious and lifelong deficit. I do not count calories or anything like that. I pay close attention to chemical makeup of foods and how that interacts with my condition.
But most people with CF are prescribed a high salt, high fat, high calorie diet. In practice, this means they are actively encouraged by medical professionals to eat a junk food diet. I went the other way. I pay very close attention to the quality of my food, not the quantity. I went looking for good quality fats and salts and other foods. I think the current practice of prescribing a junk food diet because it is high in fat and salt without caring that it is low in quality is part of what is killing people with CF.
I don't know if that does anything to cast light on the question of fats and diabetes per se. I don't think fats per se are terribly important to the process behind diabetes. I think acidosis and infection are likely more related and you see both of those at high rates in people with CF. There are also studies that clearly link inflammation and diabetes. As I said in the comment that started this subthread, I believe that likely points to infection as an underlying cause of diabetes.
Addendum: I should add that as I have gotten healthier, my appetite has shrunk. I eat a great deal less than I used to eat. Redressing the lifelong deficits dramatically reduced my need for a very high calorie diet. I probably still eat a bit more than average, but I eat a lot less than I used to.
I will add that I carefully avoid peanut oil, having found it to be extremely inflammatory. Anytime I have it, there is just hell to pay. So I will say that if people are consuming fats that promote inflammation, that would be relevant -- but not because they are fats per se, but because they have a chemical makeup that promotes the inflammation that promotes chemical derangement and infection.
You: "That is interesting to me. CF is basically a salt-wasting condition. There are various forms of defect in the CFTR, but knowing that it basically leaks may explain why it is basically a salt wasting condition."
Errr, that was referring to normal CFTR. The class of proteins it belongs to normally require ATP, the ready energy source in cells, to actively transport stuff, e.g. use up one molecule of ATP to transport one molecule of whatever. CFTR is 'broken' in that it looks a whole lot like one of these proteins, but instead of ATP being used to transport a molecule, i.e. against an osmotic gradient, the ATP just "opens its door" (or the reverse, I didn't check), and then ions and water go whichever way the gradient favors. I.e. if there's lots more water in the cell than outside the cell, it goes out.
So one of the things I found was that there are two conditions that cause higher misfolds of proteins within the cell: Derangement of PH level and derangement of salt level. You see both of these things happening with CF.
Ah, I see where there's usefulness here, given the variety of CFTR mutations (and note that one person might have two different mutations, one contributed from each parent, or arising from very early stage embryo mutations). There will be mutations that as you describe, where if you can adjust the conditions under which the protein is created and initially folds, and or preforms afterwards, you get a more favorable outcome.
As for acid, well, it depends on where the acid is. Acidosis is a condition outside the cell, per the Merck Manual "Acidosis is excessive blood acidity caused by an overabundance of acid in the blood or a loss of bicarbonate from the blood (metabolic acidosis), or by a buildup of carbon dioxide in the blood that results from poor lung function or slow breathing (respiratory acidosis)."
So to refine your hypothesis, once the protein is in the cell membrane, a greater concentration of hydronium ions (https://en.wikipedia.org/wiki/Hydronium) outside will damage it. And if the outside is more acid than the cell, they'll flow in through the channel, where they can donate a proton (bare hydrogen atom), doing mischief to CFTR or even the cell.
So I have concluded that there is a vicious positive feedback loop where the more acid you get, the more you see protein misfolds and the more you see protein misfolds, the more acid you get. I believe this is why it is a degenerative, progressive condition.
That would only happen if your as blood gets more acid, it stays more acid, but short of requiring intervention. Note also that proteins tend to? often? have have a life cycle, they get produced, work for a while, often get zapped one way or another, and then get recycled. That mutation class I mentioned of premature degradation implies this is true for CTFR; the cell would fail to keep up production sufficient to counter that. Note also there should be a signaling mechanism that tells the cell to produce more or less of CTFR, I'm assuming that even if the signal is "I really need more!", the cell has a limit to how much it can produce, and still survive, it can't under-produce other vital stuff too much ... and that also might have an effect.
Sounds like there's cumulative damage elsewhere that can't be reversed in this way, e.g. the stated pancreas scarring that causes Type 1 diabetes, or the classic clubbed fingers per the Wikipedia picture.
But most people with CF are prescribed a high salt, high fat, high calorie diet. This means they are actively encouraged by medical professionals to eat a junk food diet. I went the other way. I pay very close attention to the quality of my food, not the quantity. I went looking for good quality fats and salts and other foods. I think the current practice of prescribing a junk food diet because it is high in fat and salt without caring that it is low in quality is part of what is killing people with CF.
Well, salt is salt, and it might help to increase the saltiness of your blood (not sure how much that's possible or practical), you'll end up with more salt inside the cells (or that sounds likely, but there are surely other proteins that also can transport salt in and out), and outside the cell, the former probably not so good, the latter perhaps in balance for the best for many people.
More later if you wish when you have time, on this HN topic, or you're welcome to email me (see the address in my account info).
Yes, but it potentially reconciles the seeming contradiction between the defect causing both a bottleneck and salt wasting. Perhaps that is gibberish, but I have always wondered how a bottleneck can cause salt wasting.
As for acid, well, it depends on where the acid is. Acidosis is a condition outside the cell, per the Merck Manual "Acidosis is excessive blood acidity caused by an overabundance of acid in the blood or a loss of bicarbonate from the blood (metabolic acidosis), or by a buildup of carbon dioxide in the blood that results from poor lung function or slow breathing (respiratory acidosis)."
Well, that sounds ridiculous to me.
People with CF hoard both calcium and glutathione inside the cell. They have too little glutathione outside the cell, so some people inhale NAC to increase glutathione on the lung surface, with good results. I have tried to correct the underlying cause of those imbalances. Given that life did not emerge from the ocean until we had bones, in part because the calcium mediates the blood ph, something not needed for marine animals, and given that people with CF not only hoard calcium inside the cell but are prone to osteoporosis as early as their teens, I believe the body is using calcium and glutathione to buffer the cells against extremes of acidity and other chemical derangement.
The body does not allow the blood to get too acid unless there is serious failure somewhere. The body strips the bones of calcium to keep the blood ph within very narrow boundaries because failure to do so quickly results in death.
Therefore, it is silly to think of acidosis as something that happens in the blood. By the time the body lets the blood get too acid, something has to have gone very very badly wrong in all the tissues.
A few months ago, a woman who has written papers on CF told me I had to be wrong, that CF could not be causing severe acidosis as that would kill you because the cell can only exist within a narrow ph range. I rebutted that with "Given that CF is extremely deadly, I don't think that is a good counterargument." She then found that several years ago, there was clinical research into acidosis and CF that fits with my hypothesis.
I posit that the mental model that acidosis is about blood ph is silly and misses a larger issue.
That would only happen if your blood gets more acid, stays more acid, and so on. Note also that proteins tend to? often have have a life cycle, they get produced and recycled. That mutation class I mentioned implies this is true for CTFR, that class results in premature degradation, the cell fails to keep up production sufficient to counter that. Note also there should be a signaling mechanism that tells the cell to produce more or less of CTFR, I'm assuming that even if the signal is "not enough!", the cell has a limit to how much it can produce, and still stay alive, it can't under-produce other vital stuff too much.
Some of my handwavy recollection is that some drugs are successful in improving production of the CFTR channel and this is known to significantly reduce symptoms. If you can get the body to create more CFTR channels, you can reduce symptoms. This is clinically known and not something I am just imagining. I think it makes logical sense as an explanation for why my condition is so much more stable than I ever expected it to be. :-)
Well, salt is salt
In theory. In reality, that is a big fat NOPE. There are huge chemical differences between "table salt" which is filled with crap to make it pour easier and "canning or pickling salt" and "high brine sea salt." There are very huge chemical and qualitative differences. These differences multiply (or at least their impact on the body does) when you have a salt wasting condition and must consume higher than normal amounts of it. I stopped consuming table salt some years ago. I think it makes an excellent non-toxic household cleaner. I do not view it as edible.
My email is also in my profile if you wish to continue the discussion there.
On the other hand, my "salt is salt" comment was more about how NaCl is NaCl, wherever it comes from, table salt, McDonalds, etc., and will have the same effects regardless the source. Additives might indeed cause harm, but that won't be directly linked to NaCl once it all hits the mixmaster of your stomach.
A bit more to follow in email.
Will just briefly note that one modern therapy for CF is inhaled salt water mist and it was developed because people with CF who dive/surf/etc have better prognoses. I moved to the coast for a time to have consistent, free access to the ocean. The ocean has a lot more minerals in it than just salt. Some brands of sea salt also have a mix of those other minerals. When you dump salt, as with CF, it is going to drag other things out with it. Replenishing both the salt and the other associated minerals was important in getting myself healthier. This is largely overlooked by everyone. Everyone thinks "salt is salt" and that is true if you mean NaCl is NaCl. But products labeled "salt" almost never are just NaCl.
Good talking to you. Have a great day.
The bad science and dogma is still kicking, but I'm optimistic it will be gone within the next 5-10 years.
[1]: http://www.cdc.gov/mmwr/preview/mmwrhtml/figures/m304a3f1.gi...
Source: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5304a3.htm
"The current study adds weight to the longstanding recommendation to restrict total fat and saturated fat. While adjusting for BMI eliminates the effect, this does not mean that dietary fat is not important. It is biologically plausible that high-fat diets promote weight gain, which then promotes insulin resistance. There is a large body of evidence that supports this view."
It also references the large body of evidence that high-fat diets are associated with impaired insulin:
"A large body of experimental data generated in laboratory animals strongly supports the notion that high-fat diets are associated with impaired insulin action. It appears from animal studies that saturated fats, in particular, have the most detrimental effects. Based on this information, along with the known risks of high saturated fat intake on cardiovascular disease risk, professional organizations such as the American Diabetes Association, the American Heart Association, and the U.S. Department of Agriculture have made recommendations that Americans aim for a total fat intake of no more than 30% of calories and choose foods low in saturated fat."
I wouldn't describe it as tenuous. But this is just one review of a study. There is a lot more out there. It doesn't necessarily need to be the most recent to be substantive.
If the effect goes away when controlling for BMI, I'd say that's a pretty weak link.
A large body of experimental data generated in laboratory animals strongly supports the notion that high-fat diets are associated with impaired insulin action
"in laboratory animals"
Color me skeptical, but lots of things happen in animals that don't happen in humans. Animal studies are suggestive, but hardly conclusive.
Sound tenuous to me. But I'm also weighing that against a large body of research that suggests that high-fat, low-carb, moderate protein diets are a very healthy diet... possibly optimal for some people.
Saturated fat is categorically the same as cigarettes in the popular conscious, therefore it is not surprising that (in general) people who eat more of the stuff are unhealthy.
What does the popular conscious have to do with it? Are you suggesting that if saturated fat was considered healthy people who ate more of the stuff would be healthier?
There is a double blind study regarding this, The Minnesota Coronary Study, it found no effect to heart health or mortality by reducing saturated fat.
Among the Type 2's aggressively treating their metabolic disorder (a significant fraction whom drop out of Type 2 biomarkers and can stop taking medication, and are re-classified as insulin resistant at worst), overwhelmingly the diet used is various degrees of low carb, with some experimenting with various fasting regimens mixed in. As long as total caloric intake does not exceed one's TDEE, so far it seems daily high saturated fat consumption (like some ketogenic diets) doesn't adversely impact blood sugar nor cholesterol metrics; some advocate not subjecting the saturated fats to overly-intense heat before consumption, but actual quantity (within reason) seems immaterial as long as the carbs are cut down to fractions of what is "normally" consumed by everyone else. Sweden's national health system has collated a lot of this research and is doing a lot of their own original research; they have recently come out officially in favor of low carb.
> As long as total caloric intake does not exceed one's TDEE, so far it seems daily high saturated fat consumption (like some ketogenic diets) doesn't adversely impact blood sugar nor cholesterol metrics;
The diet does adversely effect cholesterol metrics. Take a look at the posts with lipids on /r/keto. Their cholesterol drops a bit because they lost weight, but most of them are still in the danger zone.
I'm sure you've heard of Loren Cordain, one of the leaders of the paleo movement. He is credited as an author on a paper[0] that comes to the conclusion that 50-70mg/dl of LDL is the true optimal. You can't achieve that eating a diet rich in cholesterol.
[0] http://www.ncbi.nlm.nih.gov/pubmed/15172426
> Sweden's national health system has collated a lot of this research and is doing a lot of their own original research; they have recently come out officially in favor of low carb.
Could I get a citation for that? I thought they only recommended low carb in specific situations. Why would someone who isn't obese or diabetic go on a keto diet?
[1] http://www.ncbi.nlm.nih.gov/pubmed/18615352
The context of the SBU finding for low carb was indeed for low carb and Type 2's; when I mentioned that I was still in the context you brought up of Type 2's.
[2] http://www.dietdoctor.com/swedish-expert-committee-low-carb-...
There is a lot of discussion on /r/keto and other keto forums about high cholesterol numbers, and it seems we need to perform more research. Because some (not all) longer-term (longer than a year) keto dieters are finding that their cholesterol numbers went down after staying elevated for awhile; one hypothesis is that the high numbers are from the release of cholesterol from breaking down fat stores.
[3] http://bjjcaveman.com/2013/03/10/the-effect-of-a-ketogenic-d...
Thanks for sharing the links, appreciated.
However, we can agree that there are many people who give diet-absolutes advice and are totally wrong.
But there is good advice out there too, and we shouldn't close down assuming all advice is bad advice, just because some it is bad advice.
But "too much is unhealthy" is a tautology. There are a number of studies that show that sodium-restricted diets may increase all-cause mortality. So "too much sodium...is unhealthy" is not nonsense but completely meaningless and unhelpful as advice.
We generally know much less about nutrition than is commonly portrayed.
You seem to be arguing that, because too little is harmful, saying that too much is harmful is meaningless. That seems... less than logically sound.
Or have I misunderstood you?
We know that reducing sodium may be harmful. It's possible that attempting to reduce sodium below what the average person consumes may be harmful (or may be harmful for some portion of the population). We don't know what is the "ideal" level or range of sodium.
So, yes, it is true that "too much" sodium is bad for you, but we don't really know how much is too much, or even if the amounts that people eat today are actually too much for the typical person.
The nuance required for an actionable claim sounds more like "more than x but less than y based on metabolic factors a, b, and c is the healthy range". This is difficult to construct based on existing research, thus we need to learn more before making blanket statements.
Turns out, research has now shown that such "overmanaged" patients actually fare worse than those who allow some flexibility in glucose levels.
I have a quite knowledgeable family member who has diabetes, from whom I've learned this.
As I've gotten older, I've watched a lot of... um, "best practices", in health care as in other matters, be debunked. And, in retrospect, the advice often was a matter of self-reinforcing opinion rather than demonstrated science and research results.
I am always puzzled while in the States that I can't buy anything non-low fat and barely a single brand of unsweetened yogurt even in Whole Foods; it feels like I am forced to buy only inferior food over there, guys. I then imagine your food industry extracting most of beneficial fat from milk products and selling you supplements containing those ingredients for significantly higher price...
Hmmm, over here isn't not hard to buy stuff with "healthy" amounts of fat, but, yeah, sugar abounds.
Ah, but the bacon counterrevolution is a wonderful thing ... although my favorite is Oscar Meyer, which is "sugar cured"; well, after salt, and officially ends up with 0 carbohydrates (i.e. below the reporting threshold).
So not all is lost!
The usual cycle of Greek yogurt is that new high-end brands appear with no sugar, get popular, then introduce new flavors filled with sugar. Some of them hide it in the ingredients list by calling it "evaporated cane juice", as if you didn't know what kind of cane they were talking about.
Huh? My Whole Foods has Fage (the best, IMO), Siggi's, Wallaby, and more.
Like this: http://images.costcobusinessdelivery.com/image/media/350-824...
"Polyunsaturated fat" is a bad category; it includes both omega-3 (generally considered good), omega-6 (generally considered bad), and omega-9 (generally neutral). Statements about polyunsaturated fat which fail to distinguish these have no possible hope of being correct.
What may be important is the balance between omega-3 and omega-6 in one's diet, with omega-6 ending up having negative consequences when one ingests too much simply because those same people aren't ingesting enough foods with omega-3.
Basically when speaking of food, humans have a finite capacity to eat, so if you eat too much of something, then you eat less of something else.
This may be the case for vegetables versus meat. It's generally accepted that too much meat is bad for our health, but the cause is completely unknown. And it's certainly not the fats, as we've been led to believe. Eating too much meat may be unhealthy simply because those people aren't eating enough vegetables.
Want to bet that in 4-5 years tops the current beliefs with those fatty acids will be turned on its head? There's no science that has failed us more than nutritional science. Pick any cult, any religions, any of the superstitions that have survived for hundreds or thousands of years and you've got something healthier than nutritional science because people have survived those cults and superstitions, yet it's becoming clear that nutritional science is responsible for the obesity epidemics ;-)
With that being said, refined oils high in omega-6 fats should be avoided, as all the anti-oxidants that keep them from going rancid in their whole food form are absent.
U.S. governmental regulations have long discouraged fat intake, replacing those calories largely with carbs. This was based on the assumption that the fats were harmful, rather than extra calories in general. The article is highlighting a change in understanding that will hopefully have us stop demonizing fats in favor of carbs in a diet that is otherwise within bounds calorically.
In short, we know now that it is not necessarily bad to eat fats (anymore than it's bad to over-eat in general).
I sometimes feel like at least a third of the resistance to ideas like fat is ok is based in a deep-rooted belief drilled into us by fad diets that eating healthy can't also be delicious.
Literally? Or imaginatively?
Get a variety of foods (fruits, vegetables, meats, etc), and avoid what causes you problems with digestion...
That's hard enough without going into too many specifics and would generally serve people better in general. Once you get your needed protein in, for the most part, calories are a wash... excessive sugars/carbs causes other problems over time. But trying to say you can have X and not Y is a path to failure for most.
Also, trying to keep it on a daily basis doesn't always work so well either... if I get a few days a week that I have a longer fast cycle (eating once a day), I tend to do better... But it's a matter of keeping your overall intake in relative check without dwelling on any particular piece.
Eat food, avoid processed foods, eat veggies and fruits, get a variety, don't eat too much... it's not all that hard, but that's not how people think... we've also got generations of snacking, sugary drinks, and carb/sugar laden food supplies.