#theres too many word docs im losing it

[roadyblr]

THANK THE LORD!! yechan finally posted!!!!

my prayers have been answered. my hopes have been fulfilled. my wishes granted. HES BACKKK

(and probably gonna disappear for the next month but that fine.)

his hair still needs some.. how do I say this nicely, getting used to. and honestly they couldve just bleached it. and DYED IT BACK TO RED. EVERYONE WOULDVE LOVED IT ARGHHHHHHH T-T

also, I saw my neighbours cat yesterday when I got out of the elevator (she lets him out into the hall to roam) and I pet him. her son had to take him away and lowkey in my brain I was like "DONT TAKE LINO/YECHAN FROM ME PLEASEEEE"

(he was really cute and polite and tall and muscular and he was wearing a tank top and he had dimples and a cute smile and was also way too old for me T-T)

anyways, the lady sent him (the cat) back into the hallway and I came running obviously and GUESS WHAT.

HE RAN TOWARDS ME. LIKE IT WAS SOMETHING STRAIGHT OUT OF A K-DRAMA EXCEPT IT WAS WITH A CAT AND A GIRL!!!

one of the friendliest, playful, cute kitties ive ever seen in my entire life I've lived.

SPEAKING OF CATS!!!

me and my two bestfriends did a hear me out cake and I put baymax, player 067 from squid game, dori (yes the cat), ryu sanada from kimini todoke HES SUCH A GREEN FLAG I LOVE HIM MORE THAN THE MAIN MALE LOVE INTEREST, I put lino because these were my non-kpop friends and whenever I bring up his name they roll their eyes or walk away sooo.. he's technically not a hear-me-out but in that situation he is.

i also put tricky.. don't ask, mike from stranger things but specifically in seasons 1 and 2. HE WAS SO CUTEEE. and that was it. considering my friends put SUNSETS, THE RED M&M AND SLEEK WATER BOTTLES (not in the dirty way) I think my selections were pretty good.

ive yapped way too much. love you byee!!

<3

bi monthly yechan delivery (sometimes more than bi monthly, technically there was two? he was in wa-xx that dropped today but that might not count) HE WILL BE BACK SOON DW (i have no evidence for this other than upcoming concerts)

male cats are so lovable, like out of all the ones that are in my household my grandma's is the sweestest of them all, he likes shoves his head against face for a kiss when he gets in my arms i'd die for him

your friends onto something with the sunsets, i call the moon my wife but sunsets a different breed but also hearing player 067 oh my god my heart not to off topic but that marbles game from the first season HURT, my cousin actually did a scene redraw of her

anyway roadyblr tame hear me out:

anyway-

[puppppppppy]

footnotes arent enough I need you to talk to me like im fucking Amelia Bedelia

[mushtoons]

YOU HAVE NO FUVKJN CLUE WHAT KIND OF SHIT LEONARDO HAMATO DOES TO ME. GODDAMN. theres a reason im obsessed w this boy and those reasons are Many. hes just like every other leo if they got a moment to be a person and it drive me fuckin nuts. bonkers, even. hes still analytical he still cares with all his heart hed still do anything to keep them safe and hell still do it alone he still cares about tradition and the status quo and he refuses to show that he cares both because he doesnt want to break that status quo as hes not the eldest anymore and because he doesnt want to stop being able to be carefree and happy. but hes still made up of a leader (he still wears red beneath his blue, a mask that doesnt hide a thing-and the leader wears red, doesnt he, doesnt he?) and god, hed still do anything to keep them safe. hes still the head, and the legacy, and. karai. you are not alone. and yet, both her and leo, they readily threw themselves into a prison that they thought theyd never escape from. no one is alone. except for them. because they have to, this is their duty, this is their comeuppance, they have to be a hero, they have to be the savior. and leos closeness with karai and. and when they leave karai and then when they leave raph, both times, he has to be dragged away. and he locks himself in a prison dimension. and hes calling casey 'case' by the end of the movie, and his supposed last words to him are to say hes proud. and hes so bright and kind and annoying. and. theres just. god theres so much i could say about leo. i use jokes to cope, with my last breath i told you so, hero moves are totally your style, youve been portal chopped. and he only cries in the prison dimension. the moment that portal opens he stops. and he doesnt say a thing between youve been portal chopped and. and, 'took you guys long enough'. like he knew theyd save him. and mikeys portals were a miracle. and he left a katana there. and its a belief of mine that, afterwards, hes more subdued and careful and out of the way. its not about me. and maybe he pushes that too far. and maybe, hes always worked hard to keep his hurt from them, so they dont have to bother with it. mikey needs more help, donnie is more sickly, raph is trying so hard. that last thought was off the hook idk abt that one yet dont take it too seriously. but anyways i think a lot abt him and caseys relationship too. the gentle carefulness that could bloom there alongside bright burning youth and love and hope. and casey was their final stand, and he did it. and he told him, i dont wanna lose you again. and like..just. leos everything. the masks he hides behind and the person underneath and how its clear he cares and..leo is the soul. mikey is the heart and donnie is the mind and raph is the body and leo is the soul. tuning the background noise and guiding them, quiet or loud, whatever he needs to be. and just..the way he always quietly led them and his smarts and how he got to be someone and how he still tries to throw that away and how clear it is he doesnt care for himself the way he does others and how that reflects in future leo concepts and how much I know he would care for this younger versions of himself and. and how bright he is, how annoying yet loveable and so, so interesting he is. this was so scrambled but idc i love him so much. if you want more of my coherent leo thoughts point a thing out this was summary and i DO have SO many thoughts on the prison dimension as a whole (four poems actually), casey and leos relationship (a whole post and then a much larger section in a doc), the peepaw and leo (again A WHOLE DOC for peepaw concepts), and general analysis on the boy (yet again a whole doc). also sorry if this was a bit much lmao he means a lot 2 me

DHDHDJD HOLY SHIT THIS IS A LOT /POS

LMAOOO WE CAN TELL WHO YA FAVORITE IS /LH BUT THIS IS SO DJJDJFDJDJD SO DETAILED AND JUST ❤️❤️

[trans-mink]

Istg these writer questions are all too good I want to ask you every single one but that'd be a lot so...17, 22, 34 + a question you'd really like to answer!

im so sorry this took a while things been all over the place on my end, this is going to be very all over the place but anyway

17. talk to me about the minutiae of your current wip. Tell me about the lore, the history, the detail, the things that won’t make it in the text.

uhh so i got several wips that are v much on a break but I started reworking an old arcana self insert fic of mine from 2019 cos tbh the writing is ass and I can make it sound a lot better now idk how that bitch has so many kudos on it, its not good!!

the plot is basically that the MC (reader) has chronic joint pain in the winter when its cold and Julian helps to look after them. The inspiration was that i have chronic joint pain that's way worse when its cold and i wrote it as a comfort thing lol. its still up rn in its original state but will be updated soon hopefully

my other main wip is my dmmd fic that i worked on p much all of last year but now i have burnout so im taking a break rip.

its kinda a re-write of the reconnect game but with more characters and set in my own universe but i think once i get over the bump of the main story line its gonna be more slice of life/ romance focused as a change of pace to the first half. Unlike the reconnect game i also focus on other characters that arent the main character's love interest because if i was a reader i'd wanna know what everyone else is up to post canon. It basically feels like a sandbox for me to write my character head canons lol.

22. how organized are you with your writing? describe to me your organization method, if it exists. what tools do you use? notebooks? binders? apps?

everything is in google docs, i have notes pages and a loose colour coding system going with how I edit things e.g green= published, orange= needs work/ to be changed, purple= notes about canon/ in fic lore.

Sometimes if i feel my work is getting cluttered i'll move it to a separate doc so i end up with about 3 documents that are different editing stages of the same chapter.

Theres also a "cutting room floor" doc where i put stuff that didnt make the final cut in case i wanna refer to it later and its not lost to the back space button.

34. thoughts on the oxford comma, go:

fam I dont even know what a oxford comma is, I just be putting them shits wherever feels right. Like a granny adding seasoning to her cooking.

Ok i just googled it and I dont tend to use it i dont think but honestly do whatever u want, who give a shit. language and grammar are fake.

extra question picked at random :D

12. if a genie offered you three writing wishes, what would they be? btw if you wish for more wishes the genie turns all your current wips into lorem ipsum, i don’t make the rules

first wish is to know how characters feel in response to whatever is happening to them, my biggest thing rn is being unable to put myself in their shoes and i think it would help a lot.

second is to consistently remember HOW to write well, cos i have bursts of knowing wtf im talking about but will suddenly lose it even if im in the middle of a work

third is knowing the exact word or phrase to describe scenery, emotions and facial expressions. I struggle with those the most for some reason.

[irastayshome]

Ibrahim's birth

Ibrahim arrived in this world on 21st January 2017. Back then, we were lucky to afford a doula because I was hella nervous about the whole birthing process and tbh my head wasnt in the game because of all the stress at work. After the 'hard part' was over, and as I held my son, I vividly remember my doula saying that the easy part was over and the hard part of being a parent has just begun. I thought it was a joke at the time because, well, what could be harder than pushing a 3 kg baby out of your vagina? 2 yrs and 6mths on, I have mentally kicked myself in the head for taking my doula's words lightly. These days, I consider it a win when I do not raise my voice or completely lose my sh** and raise my hands at my son. I keep needing reminders of what it took to get him into this world and the many moments we failed him along the way so that I do not be complacent and mistreat him.

So I thought I might write his birth story down after all. Didn't really wanna remember all the details of something that feels rather insignificant now, but some days at home are just rough and a good reminder is useful.

*

19 January 2017. I had been on maternity leave for a week, but only just completed my case transfers from home. My mamamia had been insisting that I sleep over her place once a week for the last trimester on Hasyali's night shifts. I didnt mind at all, because my r/s with my parents have improved significantly after moving out. Distance is truly necessary sometimes.

It finally dawned upon me that I was due in a week. Being last minute as I always am, I tried to 'catch up' on the squats that my doula/birth educator had been reminding us to do at 9 pm. But really, i was just doing it for fun cause like it would make any difference at 39 weeks, esp since ive been treating my body like crap while handing over my work the last few weeks. Planned to youtube more exercises to speed up labour etc etc but fell into the rabbit hole of "natural birth positions" and "painfree birth vlogs" and before I knew it, I was hooked on the Midwives yt tv series till i fell asleep at 5 am. Damn youtube.

20th January 2017. 7 am. Felt like I ate something so bad and had to do a big one. And so I did, groggily, and went back to sleep. Feeling so smug that I could finally sleep in on a weekday. 9 am. What is going on with my bowels??? Tried to recall what I ate last night, but dont care just sleep after the business. 10.30 am. Sat up and mentally admitted that those horrid pains at the bottom of my tummy could actually be contractions! Trying to keep cool, I ate breakfast quickly, trying to mask my ronyok face each time the tightenings came by because nyayi was there and I just did not wanna tell my family. pretty sure they would have shipped me off to the hospital immediately.

Took cab back at 12.30pm and smsed hubs about the contractions, saying it could potentially be the real thing. But not sure, so I timed them in the cab. 10 mins apart. regular. oh crap its happening. Got home, discovered the bloody show. So yup i got my confirmation. Smsed hubs a photo of it but told him to just take it easy, go solat Jumaat and just slowly pack his bag aftee. He just got off his night shift so he probably hasnt slept at all. Told doula Kak Hajjar about whats going on, and was advised to just relax and walk2 until i cant talk anymore from the pain. Hubs came back, and i took off on a birth walk alone around the estate. Every few mins, I just stopped and breathed deeply, sorely regretting not pestering my hubs to come along bcoz adoi sakit and nothing to squeeze or hold on to. and in the 3 pm sun no less.

Came back, started panicking when i realised hubs belum pack!! what is it with men and last minute packing?? feeling annoyyed bcoz im about to do some serious work but he cant even get started on packing. but ok takpe, got in the shower to cool down and to relieve the pain while he packed. Contractions were now 4 mins apart, but I could still talk. NUH told me to come in now. Doula told me to wait till i cant talk. The kancong me decided to go anyway, worried about the rush hour jam on the start of a weekend.

Arrived at NUH at 6 pm, realising that id skipped lunch. I was hungry, and oh no so damn sleepy bcoz i barely slept the night before! Damn youtube. Ate mr bean pancake with hubs. Met doula who told.me i dont look like its time bcoz i could talk and joke about. I admit i secretly thought that it was because i had a high tolerance for pain hahahaha joke. Entered the delivery ward at 7 pm, was 4 cm dilated. Yay! but wait what, all that pain and only 4 cm? oh no.

So began the longest night of my life. Doulla massaged my back and did hip squeezes through contractions, and I occasionally swayed while standing with hubs. These two were just incredible birth partners. My labour pains were rough at the front, but damn the back labour pains were friggin insane! Felt like maybe I had tentacles trying to burst out of my spine and turn into Doc Ock.

At some point, i remember just saying random supplications and feeling so regretful that i had not rehearsed what selawats I wanted to read in those moments bcoz my head was really jammed up trying to manage the pain. By 3 am my body felt like it had gone through a marathon and i really did fall asleep between contractions out of sheer exhaustion. It was exhausting to just tahan the pain.

By 4 ish am (hazy on the details by now), a VE confirmed I was 9 cm dilated. At this point I was already vomitting and my head hurt so much from tahaning the pain. I remembered thinking, or maybe even saying out loud, that I wanted them to cut the baby out. Im pretty sure I was transitioning at that point but I didnt know bcoz my mind was too panicky. They told me the head was still too high to push, so they offered to burst my waterbag, but said theres no assurance it would bring the head down but wld certainly intensify the contractions. I was pretty sure I would pass out if they intensified, out of exhaustion. and never mind that I was barely able to wake up btwn contractions due to my flu and fever (yes ARGH hate flu during labour). So I refused and waited for news that im fully dilated.

6 am. Still at 9 cm. My head was thinking "how long did Kak Hajjar say transitions lasted again?? takkan lama gini??" This time, my mental strength just gave way. I screamed for an epidural. I remember feeling so terrified that my baby would be stuck while im pushing, because I had zero energy left. Fatigued from the pain and the fever, I pleaded for an epidural again n again. I rmbr my doula, my husband, the nurses all giving me such kind words of support, saying ive gone si far and am at the last lap, and encouraged me to stick to my birth plan of going without medication. But I was too defeated by exhaustion and just wanted to sleep. Hahahaha. Like i literally said "yang, i nak tido" and started to cry.

So they called in the anesthesiologist (dunno the spelling). While he prepped the long-ass needle, I felt a huge gush of warm water down there. My waters broke. At this point I could have just waited for the head to descend, but I was too tired and looking forward to a promised 2 hour rest before pushing. So I kept quiet about it. I was in tears, out of disappointment at myself for not being able to ride out the exhaustion. But my doula was so kind and reminded me that God is the best of planners, and perhaps this was the way for me to achieve a natural birth still and avoid any emergency csection if I could not push. The nurses too were angels, and kept assuring me I had tried really hard for a long time and shouldn't beat myself up. And so I slept. That was the best 2 hour sleep of my life. pretty sure I snored and drooled, in the presence of my doula. Nak kata paiseh but nah I was too tired to care, and all modesty had left the room hours ago.

8 am. Woken up by cheerful nurses who told me it was time to start pushing. I just wanted to sleep in longer, but then I remembered oh ya baby is still inside. That epidural was gooooood. So began pushing. It felt so weird pushing when I cant feel anything moving down there. They had to tell me when to push i.e. when contractions came, and kept telling me I was pushing wrong and i had to do it as how i would when pooping. I suddenly didnt know how pooping felt like anymore. Kept pushing for an hour plus, but apparently the head keeps going back in. My husb and I had affectionately named our foetus "jubjub", just to avoid calling it the baby during the pregnancy. and my doula joked that perhaps the baby keeps going back in bcoz we named him jubjub like the muppet from Hi-5 that likes to peekaboo around. haha that was a good one.

My gynae finally came in around 9.30 am ish. She told me that I had to do an episiotomy to help push the baby out. My husband stopped her and told her to let me continue trying. But eventually she kept persisting and my husband apparently could not tahan seeing me push so hard anymore (he said the veins on my face look like they were gonna burst). So he agreed. The moment she cut, I pushed and felt the head empty out of me. I thought that was weird cause I was on epidural, but apparently they reduced the dose while pushing. A few more pushes later, I heard it. Ibrahim's first cries. The nurses and my doula congratulating me. My husband telling me I did it and he was proud of me. But mainly, Ibrahim's cries. 21st January 2017, at 10.03am.

They placed him on my chest. I cried. and cried. And i thought he was the most perfect thing I could ever hold in this world.

Dearest Ibrahim, a mother can love her husband out of choice, but theres simply no choice in this love I have for you. It is so raw and intense and relentless, that Im so consumed by it from the moment I held you. There are days, now, when I feel your anger towards me because I am so hard on you, especially since im not very good at coping with the two of you. But I hope you never feel that I love you any less when I get angry. and I hope you truly forgive me when you give me a hug after I apologise each time for beating you. You deserve so much better, and i'll keep striving to be a better mother to you and adik.

Ok bye. Am gonna cry my eyes out now. Damn birth stories.

[milenasanchezmk]

Is Keto Bad For Cholesterol?

We’ve all heard the story. Maybe we’ve even been the protagonist.

Person goes full keto. They lose a bunch of weight, normalize their pre-diabetic glucose numbers, resolve their high blood pressure readings, have more energy, feel great, and have nothing but high praise for the new way of eating.

Except for one thing, everything seems perfect: their cholesterol is sky-high. It throws a wrench into the whole operation, installs a raincloud over the procession, spoils their confidence.

“Could I be killing myself?”

“Are my health improvements just a mirage?”

In other words, are the apparent benefits of keto merely superficial if your cholesterol skyrockets?

The evidence is pretty clear that for the majority of adults who go keto, their cholesterol numbers improve.

In obese adults with type 2 diabetes, a ketogenic diet improved blood lipids and boosted fat loss compared to a low-calorie diet.

In lean, healthy adults without any weight to lose (and who didn’t lose any weight during the course of the diet), total cholesterol went up from 159 to 208 mg/dL and triglycerides fell from 107 to 79 mg/dL. A lipophobic doc might freak out at the rise in TC, but given that the triglycerides dropped, I bet the change reflects a rise in HDL and an overall positive, at worst-neutral effect.

Another study of lean adults with normal cholesterol numbers found that going keto improved their lipids, reducing triglycerides, increasing HDL, and leaving LDL unchanged. Those with small pattern B LDL particles (the “bad kind”) saw their LDL particle size increase, on average. All told, keto was beneficial.

But you aren’t everyone. You aren’t the average of a population. And, given the number of readers I have and the number of people trying a ketogenic diet, there are bound to be some people whose lipid profiles go in the other direction.

I don’t give medical advice here, and I always encourage people to partner with the physicians for health solutions. That said, let me share some thoughts on the keto-cholesterol question….

I’m not just talking about high total cholesterol or high LDL-C. I’m talking about what appears to be the real, legit risk factor for a cardiac event: elevated LDL particle number. According to experts like Dr. Peter Attia and Dr. Chris Masterjohn, atherosclerosis occurs when LDL particles infiltrate the endothelial lining of our arteries. Thus, it’s not high LDL cholesterol that increases the risk of atherosclerosis—LDL-C is the cholesterol found inside the particles— it’s a high number of LDL particles in circulation. The more LDL-P, the greater the chance of them becoming oxidized and infiltrating the arterial wall. There are many factors to consider, like oxidative stress, inflammation, and fatty acid composition of the LDL particles, but all else being equal, a greater number of LDL particles seems to increase the risk of a heart attack.

What Could Be Causing LDL Elevations On Keto? Weight Loss

I asked Dr. Cate Shanahan for her input on this topic, and she provided a beautiful explanation:

But when you stop eating so many carbs insulin politely steps aside, and your insulin levels plummet. Now your body fat can more easily and more often release its stores of fatty acids into your bloodstream.

When your body fat releases stored fatty acids, any unused fatty acids quickly get picked up by the liver and packed into VLDL lipoprotein. VLDL is a precursor to LDL. So in reducing your insulin levels and increasing your body’s use of fat, you will raise your VLDL, LDL and total cholesterol. You are simply trafficking in fat more often now. And now, because your body stabilizes fat carrying lipoproteins with cholesterol, there is a need for more cholesterol in your blood. These are not bad consequences. They are in fact happy signs your diet is doing what its supposed to be doing.

If you’re actively losing weight, you will probably experience a rise in cholesterol. This is the transient hypercholesterolemia of major weight loss, and it’s a well-known phenomenon. Once your weight stabilizes, cholesterol should normalize—although to a lesser extent than other diets, given Dr. Cate Shanahan’s explanation of increased “trafficking in fat.”

Low Thyroid Function

The thyroid is a barometer for your energy status. If you have plentiful energy to spare, thyroid function is normal. If your body perceives low energy availability, thyroid function may down-regulate. Since the thyroid plays a big role in regulation of LDL receptor activity, its downregulation can lower LDL receptor sites. Fewer LDL-receptors clear LDL particles from the blood. Folks with genetic predispositions to heart disease often have low LDL receptor activity, causing elevated LDL particles. Folks with genetic variants that increase the activity and expression of LDL receptors have lower heart disease rates. Although genes often have different effects that may affect disease risk via other pathways, that’s pretty strong evidence that LDL receptor activity regulates, at least in part, one’s LDL-P and heart disease risk.

Read this post for maintaining thyroid function on keto, and check out Elle Russ’ Paleo Thyroid Solution for an even deeper, more thorough dive into thyroid health.

Eating Too Damn Much

Some keto people pride themselves on gorging. Some are doing it for a good cause—a quest to find the fabled metabolic advantage. Some are doing it to show off and for keto cred—look how much salami I can eat! Some are using keto to deal with unresolved issues with food itself.

Everything I say about doing keto presupposes that you are eating like a normal person. You’re eating as much as you need to fuel your brain and daily activities, fitness and performance goals. You’re leaving the table satiated, not stuffed. For most people, this happens without even trying. It’s why keto is so effective for weight loss.

Genetic Variance

Genes aren’t destiny, but they do modify and regulate our response to a given environmental input.

Some people are dietary cholesterol hyper responders. Unlike the majority of the population, they absorb tons of dietary cholesterol and do not down-regulate their endogenous production to accommodate. The result is an increase in cholesterol synthesis and absorption, leading to a spike in blood cholesterol.

Some people are sensitive to saturated fat. In response to it, they produce elevated numbers of LDL particles. If your keto diet is high in saturated fat and you have a genetic sensitivity to it, your cholesterol will probably skyrocket.

Some people have genes that reduce the activity of their LDL receptors. This will necessarily boost LDL particle numbers.

This topic—genetic variance and how it affects keto—could be an entirely separate post, so I’ll leave it at that (and probably come back to it in the future).

Too Much Butter

Huh? Too much butter, Sisson? Is such a thing even possible?

Maybe. Subjecting cream to the butter-making process strips it of something called milk fat globule membrane (MFGM). And when you compare equal amounts of dairy fat through either cream (with MFGM intact) or butter oil (with MFGM absent), you get very different metabolic effects. Those who ate 40 grams of dairy fat through butter oil saw their lipids worsen, including ApoB, a surrogate for LDL particle number. Those who ate 40 grams of dairy fat through cream saw their lipids unchanged, and in the case of ApoB even improve.  That’s 4 tablespoons of butter compared to 4 ounces, or a half cup, of heavy cream.

Caveats apply here. The subjects weren’t eating a low-carb or ketogenic diet; they just added the butter or cream on top of their normal diet. But in keto people who are genetically susceptible, huge amounts of butter may be responsible for rising LDL-P.

I still love butter. It doesn’t affect my lipids like that. But your mileage may vary, and it’s something to think about if you’re in that situation.

For what it’s worth, whole food dairy like full-fat yogurt, kefir, and cheese do not have the same effect on lipids as butter. They also happen to be keto-friendly and more nutrient-dense.

So, What Can You Do If You See An Increase in LDL? Start Chugging Soybean Oil

Kidding… It’s true that swapping out some of your animal fats for polyunsaturated seed oils will almost certainly lower your cholesterol levels. It does this by increasing LDL receptor activity, but, being far more unstable than other fats, omega-6 PUFAs also increase the tendency of the LDL particles to oxidize. And since oxidized LDL are the ones that end up wedging in the arterial walls and causing issues, loading up on PUFAs might not be the right path.

You know what just occurred to me? This is an aside, but maybe linoleic acid (the primary fatty acid in seed oils) up-regulates LDL-R activity because the body recognizes the inherent instability of linoleic acid-enriched LDL particles and wants to clear them out before they can cause trouble. I hope some researchers take this idea further.

Stop Being a Keto Caricature.

Half a package of cream cheese for a snack.

Dipping an entire stick of pepperoni into homemade alfredo sauce and calling it dinner.

I’m not saying cream cheese is bad. It’s great. Nor am I suggesting you never eat pepperoni, dipped in alfredo sauce or not. But the amounts are unreasonable. And turning those into regular meals is a bad idea. There’s no reason you can’t go keto while eating a hamburger patty or ribeye over a Big Ass Salad. Far more nutrients, far more micronutrients, and it tastes way better.

Eat Less

Maybe if you’re a nomadic horselord sweeping across Europe in the early Bronze Age, you need to eat an entire lamb intestine stuffed with marrow and organs, and you should wash it down with a quart of creamy mare milk. Such a meal would provide the calories you need to see your enemies driven before you and go great with the lamentations of their women. But you’re not a Yamnaya nomad. You’re you.

You probably don’t need that much food, that many calories, and that much fat—since there’s plenty of it on your body already, waiting to be liberated and converted into energy.  Therein lies the beauty of keto. That’s what this is all about: Getting better at burning your own body fat.

Balance Your Fats

The overzealous and protracted drive to demonize all sources of saturated fat as evil has led to a vociferous backlash from the other direction. But just because the supposed experts got the saturated fat issue wrong doesn’t mean the opposite is true: That all the fat we eat should be as saturated as possible.

For one thing, eating nothing but saturated fat is very hard to do using whole foods. Very few animals exist in the world, past or present, with only saturated fat. The only exception I can recall is the coconut, a curious sort of beast that spends most of its time hanging from a tree impersonating a large hairy drupe. Your average slab of beef fat runs about 50% saturated fat, 45% monounsaturated fat, and 5% PUFA. That differs from cut to cut and depending on the diet of the animal, but not by much. It’s similar for other ruminants like bison and lamb. And the most prominent saturated fatty acid in ruminant fat is stearic acid, a fat that converts to monounsaturated oleic acid in the body and has an effect on cholesterol indistinguishable from MUFA or PUFA.

Or take the fatty acid composition of game meat—the type humans encountered and consumed for our entire history.

African kudu (antelope family): 35% SFA, 24% MUFA, 39% PUFA

African impala (antelope family): 51% SFA, 15% MUFA, 33% PUFA

Elk: roughly 40% SFA, 30% MUFA, 30% PUFA

Moose: roughly 33% SFA, 33% MUFA, 33% PUFA

I could go on, but you get the idea: Humans have been consuming a wide range of fatty acids for millennia. It probably makes sense to emulate that intake.

Once again, the folks whose cholesterol goes nuts on keto are outnumbered by those whose cholesterol improves. But if you’re one of the unlucky ones in the former category, try broadening your fatty acid intake (to, ahem, possibly include more nuts):

Focus on monounsaturated fats and fat from meat, rather than isolated sources of saturated fat like butter and coconut oil. You probably don’t have to eliminate those fats. Just don’t make them the centerpiece of your diet.

Eat more avocados, avocado oil, olives, olive oil, and mac nuts for monounsaturated fat. Salads are a great nutrient-dense way to incorporate high-MUFA foods.

Eat more fish. A couple portions of farmed Atlantic salmon were enough to improve LDL-P in overweight men and women. And compared to plain keto, keto + omega-3s from fish has a superior effect on inflammation and metabolic health.

Eat more kudu and impala (if you can get it). Sort of kidding. But really, eat them if you can.

They even have a version of keto called the Spanish ketogenic diet, which features a lot of extra virgin olive oil, olives, fish, and red wine. It works great and might be a good alternative for people whose cholesterol goes wild on saturated fat-heavy keto.

Are Traditional Lipid Markers Even Relevant for Keto Dieters?

Maybe, maybe not.

But be honest about it. You can’t oscillate between championing positive changes to blood lipids on a keto diet and pooh-poohing negative changes to blood lipids on a keto diet.

You can’t use positive changes to prove the efficacy and safety of the ketogenic diet, then turn around and claim that negative changes don’t count because keto dieters are understudied. What if those “positive” changes are actually negative in the context of a ketogenic metabolism? After all, keto dieters are largely understudied in both directions. If what’s unhealthy in a normal dieter might be healthy in a keto dieter, what’s healthy in a normal dieter may be unhealthy in a keto dieter.

I write these things as a strong proponent of spending a significant time in ketosis. As someone who frequently hangs out in a ketogenic state. As someone who wrote a book about keto and is writing another. But also as someone who insists on maintaining strict intellectual honesty and integrity.

We simply don’t know what very high cholesterol numbers mean in the subset of ketogenic dieters who experience them. I strongly suggest not being too flippant about them. 

True: There aren’t any perfect studies examining the utility of conventional cardiovascular risk factors in people eating the type of keto diets you see in the ancestral health space. Maybe your elevated LDL particle number doesn’t mean what it means in the average overweight adult eating the Standard American Diet. Maybe your inflammation is low enough that the risk of atherosclerosis and oxidative modification of LDL is low. But I wouldn’t take that risk, not until we have more data.

What do you think, folks? How did keto affect your blood lipids? Did you make any changes, and if so, did they work? Thanks for stopping in today.

Note: This information isn’t intended as and shouldn’t be considered medical advice. Always consult your doctor in the management or treatment of any health issue.

References:

Hussain TA, Mathew TC, Dashti AA, Asfar S, Al-zaid N, Dashti HM. Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes. Nutrition. 2012;28(10):1016-21.

Phinney SD, Tang AB, Waggoner CR, Tezanos-pinto RG, Davis PA. The transient hypercholesterolemia of major weight loss. Am J Clin Nutr. 1991;53(6):1404-10.

Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metab Clin Exp. 1983;32(8):757-68.

Kleinveld HA, Naber AH, Stalenhoef AF, Demacker PN. Oxidation resistance, oxidation rate, and extent of oxidation of human low-density lipoprotein depend on the ratio of oleic acid content to linoleic acid content: studies in vitamin E deficient subjects. Free Radic Biol Med. 1993;15(3):273-80.

Rosqvist F, Smedman A, Lindmark-månsson H, et al. Potential role of milk fat globule membrane in modulating plasma lipoproteins, gene expression, and cholesterol metabolism in humans: a randomized study. Am J Clin Nutr. 2015;102(1):20-30.

Raatz SK, Johnson LK, Rosenberger TA, Picklo MJ. Twice weekly intake of farmed Atlantic salmon (Salmo salar) positively influences lipoprotein concentration and particle size in overweight men and women. Nutr Res. 2016;36(9):899-906.

De luis D, Domingo JC, Izaola O, Casanueva FF, Bellido D, Sajoux I. Effect of DHA supplementation in a very low-calorie ketogenic diet in the treatment of obesity: a randomized clinical trial. Endocrine. 2016;54(1):111-122.

Pérez-guisado J, Muñoz-serrano A. A pilot study of the Spanish Ketogenic Mediterranean Diet: an effective therapy for the metabolic syndrome. J Med Food. 2011;14(7-8):681-7.

The post Is Keto Bad For Cholesterol? appeared first on Mark's Daily Apple.

[fishermariawo]

Is Keto Bad For Cholesterol?

We’ve all heard the story. Maybe we’ve even been the protagonist.

Person goes full keto. They lose a bunch of weight, normalize their pre-diabetic glucose numbers, resolve their high blood pressure readings, have more energy, feel great, and have nothing but high praise for the new way of eating.

Except for one thing, everything seems perfect: their cholesterol is sky-high. It throws a wrench into the whole operation, installs a raincloud over the procession, spoils their confidence.

“Could I be killing myself?”

“Are my health improvements just a mirage?”

In other words, are the apparent benefits of keto merely superficial if your cholesterol skyrockets?

The evidence is pretty clear that for the majority of adults who go keto, their cholesterol numbers improve.

In obese adults with type 2 diabetes, a ketogenic diet improved blood lipids and boosted fat loss compared to a low-calorie diet.

In lean, healthy adults without any weight to lose (and who didn’t lose any weight during the course of the diet), total cholesterol went up from 159 to 208 mg/dL and triglycerides fell from 107 to 79 mg/dL. A lipophobic doc might freak out at the rise in TC, but given that the triglycerides dropped, I bet the change reflects a rise in HDL and an overall positive, at worst-neutral effect.

Another study of lean adults with normal cholesterol numbers found that going keto improved their lipids, reducing triglycerides, increasing HDL, and leaving LDL unchanged. Those with small pattern B LDL particles (the “bad kind”) saw their LDL particle size increase, on average. All told, keto was beneficial.

But you aren’t everyone. You aren’t the average of a population. And, given the number of readers I have and the number of people trying a ketogenic diet, there are bound to be some people whose lipid profiles go in the other direction.

I don’t give medical advice here, and I always encourage people to partner with the physicians for health solutions. That said, let me share some thoughts on the keto-cholesterol question….

I’m not just talking about high total cholesterol or high LDL-C. I’m talking about what appears to be the real, legit risk factor for a cardiac event: elevated LDL particle number. According to experts like Dr. Peter Attia and Dr. Chris Masterjohn, atherosclerosis occurs when LDL particles infiltrate the endothelial lining of our arteries. Thus, it’s not high LDL cholesterol that increases the risk of atherosclerosis—LDL-C is the cholesterol found inside the particles— it’s a high number of LDL particles in circulation. The more LDL-P, the greater the chance of them becoming oxidized and infiltrating the arterial wall. There are many factors to consider, like oxidative stress, inflammation, and fatty acid composition of the LDL particles, but all else being equal, a greater number of LDL particles seems to increase the risk of a heart attack.

What Could Be Causing LDL Elevations On Keto? Weight Loss

I asked Dr. Cate Shanahan for her input on this topic, and she provided a beautiful explanation:

But when you stop eating so many carbs insulin politely steps aside, and your insulin levels plummet. Now your body fat can more easily and more often release its stores of fatty acids into your bloodstream.

When your body fat releases stored fatty acids, any unused fatty acids quickly get picked up by the liver and packed into VLDL lipoprotein. VLDL is a precursor to LDL. So in reducing your insulin levels and increasing your body’s use of fat, you will raise your VLDL, LDL and total cholesterol. You are simply trafficking in fat more often now. And now, because your body stabilizes fat carrying lipoproteins with cholesterol, there is a need for more cholesterol in your blood. These are not bad consequences. They are in fact happy signs your diet is doing what its supposed to be doing.

If you’re actively losing weight, you will probably experience a rise in cholesterol. This is the transient hypercholesterolemia of major weight loss, and it’s a well-known phenomenon. Once your weight stabilizes, cholesterol should normalize—although to a lesser extent than other diets, given Dr. Cate Shanahan’s explanation of increased “trafficking in fat.”

Low Thyroid Function

The thyroid is a barometer for your energy status. If you have plentiful energy to spare, thyroid function is normal. If your body perceives low energy availability, thyroid function may down-regulate. Since the thyroid plays a big role in regulation of LDL receptor activity, its downregulation can lower LDL receptor sites. Fewer LDL-receptors clear LDL particles from the blood. Folks with genetic predispositions to heart disease often have low LDL receptor activity, causing elevated LDL particles. Folks with genetic variants that increase the activity and expression of LDL receptors have lower heart disease rates. Although genes often have different effects that may affect disease risk via other pathways, that’s pretty strong evidence that LDL receptor activity regulates, at least in part, one’s LDL-P and heart disease risk.

Read this post for maintaining thyroid function on keto, and check out Elle Russ’ Paleo Thyroid Solution for an even deeper, more thorough dive into thyroid health.

Eating Too Damn Much

Some keto people pride themselves on gorging. Some are doing it for a good cause—a quest to find the fabled metabolic advantage. Some are doing it to show off and for keto cred—look how much salami I can eat! Some are using keto to deal with unresolved issues with food itself.

Everything I say about doing keto presupposes that you are eating like a normal person. You’re eating as much as you need to fuel your brain and daily activities, fitness and performance goals. You’re leaving the table satiated, not stuffed. For most people, this happens without even trying. It’s why keto is so effective for weight loss.

Genetic Variance

Genes aren’t destiny, but they do modify and regulate our response to a given environmental input.

Some people are dietary cholesterol hyper responders. Unlike the majority of the population, they absorb tons of dietary cholesterol and do not down-regulate their endogenous production to accommodate. The result is an increase in cholesterol synthesis and absorption, leading to a spike in blood cholesterol.

Some people are sensitive to saturated fat. In response to it, they produce elevated numbers of LDL particles. If your keto diet is high in saturated fat and you have a genetic sensitivity to it, your cholesterol will probably skyrocket.

Some people have genes that reduce the activity of their LDL receptors. This will necessarily boost LDL particle numbers.

This topic—genetic variance and how it affects keto—could be an entirely separate post, so I’ll leave it at that (and probably come back to it in the future).

Too Much Butter

Huh? Too much butter, Sisson? Is such a thing even possible?

Maybe. Subjecting cream to the butter-making process strips it of something called milk fat globule membrane (MFGM). And when you compare equal amounts of dairy fat through either cream (with MFGM intact) or butter oil (with MFGM absent), you get very different metabolic effects. Those who ate 40 grams of dairy fat through butter oil saw their lipids worsen, including ApoB, a surrogate for LDL particle number. Those who ate 40 grams of dairy fat through cream saw their lipids unchanged, and in the case of ApoB even improve.  That’s 4 tablespoons of butter compared to 4 ounces, or a half cup, of heavy cream.

Caveats apply here. The subjects weren’t eating a low-carb or ketogenic diet; they just added the butter or cream on top of their normal diet. But in keto people who are genetically susceptible, huge amounts of butter may be responsible for rising LDL-P.

I still love butter. It doesn’t affect my lipids like that. But your mileage may vary, and it’s something to think about if you’re in that situation.

For what it’s worth, whole food dairy like full-fat yogurt, kefir, and cheese do not have the same effect on lipids as butter. They also happen to be keto-friendly and more nutrient-dense.

So, What Can You Do If You See An Increase in LDL? Start Chugging Soybean Oil

Kidding… It’s true that swapping out some of your animal fats for polyunsaturated seed oils will almost certainly lower your cholesterol levels. It does this by increasing LDL receptor activity, but, being far more unstable than other fats, omega-6 PUFAs also increase the tendency of the LDL particles to oxidize. And since oxidized LDL are the ones that end up wedging in the arterial walls and causing issues, loading up on PUFAs might not be the right path.

You know what just occurred to me? This is an aside, but maybe linoleic acid (the primary fatty acid in seed oils) up-regulates LDL-R activity because the body recognizes the inherent instability of linoleic acid-enriched LDL particles and wants to clear them out before they can cause trouble. I hope some researchers take this idea further.

Stop Being a Keto Caricature.

Half a package of cream cheese for a snack.

Dipping an entire stick of pepperoni into homemade alfredo sauce and calling it dinner.

I’m not saying cream cheese is bad. It’s great. Nor am I suggesting you never eat pepperoni, dipped in alfredo sauce or not. But the amounts are unreasonable. And turning those into regular meals is a bad idea. There’s no reason you can’t go keto while eating a hamburger patty or ribeye over a Big Ass Salad. Far more nutrients, far more micronutrients, and it tastes way better.

Eat Less

Maybe if you’re a nomadic horselord sweeping across Europe in the early Bronze Age, you need to eat an entire lamb intestine stuffed with marrow and organs, and you should wash it down with a quart of creamy mare milk. Such a meal would provide the calories you need to see your enemies driven before you and go great with the lamentations of their women. But you’re not a Yamnaya nomad. You’re you.

You probably don’t need that much food, that many calories, and that much fat—since there’s plenty of it on your body already, waiting to be liberated and converted into energy.  Therein lies the beauty of keto. That’s what this is all about: Getting better at burning your own body fat.

Balance Your Fats

The overzealous and protracted drive to demonize all sources of saturated fat as evil has led to a vociferous backlash from the other direction. But just because the supposed experts got the saturated fat issue wrong doesn’t mean the opposite is true: That all the fat we eat should be as saturated as possible.

For one thing, eating nothing but saturated fat is very hard to do using whole foods. Very few animals exist in the world, past or present, with only saturated fat. The only exception I can recall is the coconut, a curious sort of beast that spends most of its time hanging from a tree impersonating a large hairy drupe. Your average slab of beef fat runs about 50% saturated fat, 45% monounsaturated fat, and 5% PUFA. That differs from cut to cut and depending on the diet of the animal, but not by much. It’s similar for other ruminants like bison and lamb. And the most prominent saturated fatty acid in ruminant fat is stearic acid, a fat that converts to monounsaturated oleic acid in the body and has an effect on cholesterol indistinguishable from MUFA or PUFA.

Or take the fatty acid composition of game meat—the type humans encountered and consumed for our entire history.

African kudu (antelope family): 35% SFA, 24% MUFA, 39% PUFA

African impala (antelope family): 51% SFA, 15% MUFA, 33% PUFA

Elk: roughly 40% SFA, 30% MUFA, 30% PUFA

Moose: roughly 33% SFA, 33% MUFA, 33% PUFA

I could go on, but you get the idea: Humans have been consuming a wide range of fatty acids for millennia. It probably makes sense to emulate that intake.

Once again, the folks whose cholesterol goes nuts on keto are outnumbered by those whose cholesterol improves. But if you’re one of the unlucky ones in the former category, try broadening your fatty acid intake (to, ahem, possibly include more nuts):

Focus on monounsaturated fats and fat from meat, rather than isolated sources of saturated fat like butter and coconut oil. You probably don’t have to eliminate those fats. Just don’t make them the centerpiece of your diet.

Eat more avocados, avocado oil, olives, olive oil, and mac nuts for monounsaturated fat. Salads are a great nutrient-dense way to incorporate high-MUFA foods.

Eat more fish. A couple portions of farmed Atlantic salmon were enough to improve LDL-P in overweight men and women. And compared to plain keto, keto + omega-3s from fish has a superior effect on inflammation and metabolic health.

Eat more kudu and impala (if you can get it). Sort of kidding. But really, eat them if you can.

They even have a version of keto called the Spanish ketogenic diet, which features a lot of extra virgin olive oil, olives, fish, and red wine. It works great and might be a good alternative for people whose cholesterol goes wild on saturated fat-heavy keto.

Are Traditional Lipid Markers Even Relevant for Keto Dieters?

Maybe, maybe not.

But be honest about it. You can’t oscillate between championing positive changes to blood lipids on a keto diet and pooh-poohing negative changes to blood lipids on a keto diet.

You can’t use positive changes to prove the efficacy and safety of the ketogenic diet, then turn around and claim that negative changes don’t count because keto dieters are understudied. What if those “positive” changes are actually negative in the context of a ketogenic metabolism? After all, keto dieters are largely understudied in both directions. If what’s unhealthy in a normal dieter might be healthy in a keto dieter, what’s healthy in a normal dieter may be unhealthy in a keto dieter.

I write these things as a strong proponent of spending a significant time in ketosis. As someone who frequently hangs out in a ketogenic state. As someone who wrote a book about keto and is writing another. But also as someone who insists on maintaining strict intellectual honesty and integrity.

We simply don’t know what very high cholesterol numbers mean in the subset of ketogenic dieters who experience them. I strongly suggest not being too flippant about them. 

True: There aren’t any perfect studies examining the utility of conventional cardiovascular risk factors in people eating the type of keto diets you see in the ancestral health space. Maybe your elevated LDL particle number doesn’t mean what it means in the average overweight adult eating the Standard American Diet. Maybe your inflammation is low enough that the risk of atherosclerosis and oxidative modification of LDL is low. But I wouldn’t take that risk, not until we have more data.

What do you think, folks? How did keto affect your blood lipids? Did you make any changes, and if so, did they work? Thanks for stopping in today.

Note: This information isn’t intended as and shouldn’t be considered medical advice. Always consult your doctor in the management or treatment of any health issue.

References:

Hussain TA, Mathew TC, Dashti AA, Asfar S, Al-zaid N, Dashti HM. Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes. Nutrition. 2012;28(10):1016-21.

Phinney SD, Tang AB, Waggoner CR, Tezanos-pinto RG, Davis PA. The transient hypercholesterolemia of major weight loss. Am J Clin Nutr. 1991;53(6):1404-10.

Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metab Clin Exp. 1983;32(8):757-68.

Kleinveld HA, Naber AH, Stalenhoef AF, Demacker PN. Oxidation resistance, oxidation rate, and extent of oxidation of human low-density lipoprotein depend on the ratio of oleic acid content to linoleic acid content: studies in vitamin E deficient subjects. Free Radic Biol Med. 1993;15(3):273-80.

Rosqvist F, Smedman A, Lindmark-månsson H, et al. Potential role of milk fat globule membrane in modulating plasma lipoproteins, gene expression, and cholesterol metabolism in humans: a randomized study. Am J Clin Nutr. 2015;102(1):20-30.

Raatz SK, Johnson LK, Rosenberger TA, Picklo MJ. Twice weekly intake of farmed Atlantic salmon (Salmo salar) positively influences lipoprotein concentration and particle size in overweight men and women. Nutr Res. 2016;36(9):899-906.

De luis D, Domingo JC, Izaola O, Casanueva FF, Bellido D, Sajoux I. Effect of DHA supplementation in a very low-calorie ketogenic diet in the treatment of obesity: a randomized clinical trial. Endocrine. 2016;54(1):111-122.

Pérez-guisado J, Muñoz-serrano A. A pilot study of the Spanish Ketogenic Mediterranean Diet: an effective therapy for the metabolic syndrome. J Med Food. 2011;14(7-8):681-7.

The post Is Keto Bad For Cholesterol? appeared first on Mark's Daily Apple.

[watsonrodriquezie]

Is Keto Bad For Cholesterol?

We’ve all heard the story. Maybe we’ve even been the protagonist.

Person goes full keto. They lose a bunch of weight, normalize their pre-diabetic glucose numbers, resolve their high blood pressure readings, have more energy, feel great, and have nothing but high praise for the new way of eating.

Except for one thing, everything seems perfect: their cholesterol is sky-high. It throws a wrench into the whole operation, installs a raincloud over the procession, spoils their confidence.

“Could I be killing myself?”

“Are my health improvements just a mirage?”

In other words, are the apparent benefits of keto merely superficial if your cholesterol skyrockets?

The evidence is pretty clear that for the majority of adults who go keto, their cholesterol numbers improve.

In obese adults with type 2 diabetes, a ketogenic diet improved blood lipids and boosted fat loss compared to a low-calorie diet.

In lean, healthy adults without any weight to lose (and who didn’t lose any weight during the course of the diet), total cholesterol went up from 159 to 208 mg/dL and triglycerides fell from 107 to 79 mg/dL. A lipophobic doc might freak out at the rise in TC, but given that the triglycerides dropped, I bet the change reflects a rise in HDL and an overall positive, at worst-neutral effect.

Another study of lean adults with normal cholesterol numbers found that going keto improved their lipids, reducing triglycerides, increasing HDL, and leaving LDL unchanged. Those with small pattern B LDL particles (the “bad kind”) saw their LDL particle size increase, on average. All told, keto was beneficial.

But you aren’t everyone. You aren’t the average of a population. And, given the number of readers I have and the number of people trying a ketogenic diet, there are bound to be some people whose lipid profiles go in the other direction.

I don’t give medical advice here, and I always encourage people to partner with the physicians for health solutions. That said, let me share some thoughts on the keto-cholesterol question….

I’m not just talking about high total cholesterol or high LDL-C. I’m talking about what appears to be the real, legit risk factor for a cardiac event: elevated LDL particle number. According to experts like Dr. Peter Attia and Dr. Chris Masterjohn, atherosclerosis occurs when LDL particles infiltrate the endothelial lining of our arteries. Thus, it’s not high LDL cholesterol that increases the risk of atherosclerosis—LDL-C is the cholesterol found inside the particles— it’s a high number of LDL particles in circulation. The more LDL-P, the greater the chance of them becoming oxidized and infiltrating the arterial wall. There are many factors to consider, like oxidative stress, inflammation, and fatty acid composition of the LDL particles, but all else being equal, a greater number of LDL particles seems to increase the risk of a heart attack.

What Could Be Causing LDL Elevations On Keto? Weight Loss

I asked Dr. Cate Shanahan for her input on this topic, and she provided a beautiful explanation:

But when you stop eating so many carbs insulin politely steps aside, and your insulin levels plummet. Now your body fat can more easily and more often release its stores of fatty acids into your bloodstream.

When your body fat releases stored fatty acids, any unused fatty acids quickly get picked up by the liver and packed into VLDL lipoprotein. VLDL is a precursor to LDL. So in reducing your insulin levels and increasing your body’s use of fat, you will raise your VLDL, LDL and total cholesterol. You are simply trafficking in fat more often now. And now, because your body stabilizes fat carrying lipoproteins with cholesterol, there is a need for more cholesterol in your blood. These are not bad consequences. They are in fact happy signs your diet is doing what its supposed to be doing.

If you’re actively losing weight, you will probably experience a rise in cholesterol. This is the transient hypercholesterolemia of major weight loss, and it’s a well-known phenomenon. Once your weight stabilizes, cholesterol should normalize—although to a lesser extent than other diets, given Dr. Cate Shanahan’s explanation of increased “trafficking in fat.”

Low Thyroid Function

The thyroid is a barometer for your energy status. If you have plentiful energy to spare, thyroid function is normal. If your body perceives low energy availability, thyroid function may down-regulate. Since the thyroid plays a big role in regulation of LDL receptor activity, its downregulation can lower LDL receptor sites. Fewer LDL-receptors clear LDL particles from the blood. Folks with genetic predispositions to heart disease often have low LDL receptor activity, causing elevated LDL particles. Folks with genetic variants that increase the activity and expression of LDL receptors have lower heart disease rates. Although genes often have different effects that may affect disease risk via other pathways, that’s pretty strong evidence that LDL receptor activity regulates, at least in part, one’s LDL-P and heart disease risk.

Read this post for maintaining thyroid function on keto, and check out Elle Russ’ Paleo Thyroid Solution for an even deeper, more thorough dive into thyroid health.

Eating Too Damn Much

Some keto people pride themselves on gorging. Some are doing it for a good cause—a quest to find the fabled metabolic advantage. Some are doing it to show off and for keto cred—look how much salami I can eat! Some are using keto to deal with unresolved issues with food itself.

Everything I say about doing keto presupposes that you are eating like a normal person. You’re eating as much as you need to fuel your brain and daily activities, fitness and performance goals. You’re leaving the table satiated, not stuffed. For most people, this happens without even trying. It’s why keto is so effective for weight loss.

Genetic Variance

Genes aren’t destiny, but they do modify and regulate our response to a given environmental input.

Some people are dietary cholesterol hyper responders. Unlike the majority of the population, they absorb tons of dietary cholesterol and do not down-regulate their endogenous production to accommodate. The result is an increase in cholesterol synthesis and absorption, leading to a spike in blood cholesterol.

Some people are sensitive to saturated fat. In response to it, they produce elevated numbers of LDL particles. If your keto diet is high in saturated fat and you have a genetic sensitivity to it, your cholesterol will probably skyrocket.

Some people have genes that reduce the activity of their LDL receptors. This will necessarily boost LDL particle numbers.

This topic—genetic variance and how it affects keto—could be an entirely separate post, so I’ll leave it at that (and probably come back to it in the future).

Too Much Butter

Huh? Too much butter, Sisson? Is such a thing even possible?

Maybe. Subjecting cream to the butter-making process strips it of something called milk fat globule membrane (MFGM). And when you compare equal amounts of dairy fat through either cream (with MFGM intact) or butter oil (with MFGM absent), you get very different metabolic effects. Those who ate 40 grams of dairy fat through butter oil saw their lipids worsen, including ApoB, a surrogate for LDL particle number. Those who ate 40 grams of dairy fat through cream saw their lipids unchanged, and in the case of ApoB even improve.  That’s 4 tablespoons of butter compared to 4 ounces, or a half cup, of heavy cream.

Caveats apply here. The subjects weren’t eating a low-carb or ketogenic diet; they just added the butter or cream on top of their normal diet. But in keto people who are genetically susceptible, huge amounts of butter may be responsible for rising LDL-P.

I still love butter. It doesn’t affect my lipids like that. But your mileage may vary, and it’s something to think about if you’re in that situation.

For what it’s worth, whole food dairy like full-fat yogurt, kefir, and cheese do not have the same effect on lipids as butter. They also happen to be keto-friendly and more nutrient-dense.

So, What Can You Do If You See An Increase in LDL? Start Chugging Soybean Oil

Kidding… It’s true that swapping out some of your animal fats for polyunsaturated seed oils will almost certainly lower your cholesterol levels. It does this by increasing LDL receptor activity, but, being far more unstable than other fats, omega-6 PUFAs also increase the tendency of the LDL particles to oxidize. And since oxidized LDL are the ones that end up wedging in the arterial walls and causing issues, loading up on PUFAs might not be the right path.

You know what just occurred to me? This is an aside, but maybe linoleic acid (the primary fatty acid in seed oils) up-regulates LDL-R activity because the body recognizes the inherent instability of linoleic acid-enriched LDL particles and wants to clear them out before they can cause trouble. I hope some researchers take this idea further.

Stop Being a Keto Caricature.

Half a package of cream cheese for a snack.

Dipping an entire stick of pepperoni into homemade alfredo sauce and calling it dinner.

I’m not saying cream cheese is bad. It’s great. Nor am I suggesting you never eat pepperoni, dipped in alfredo sauce or not. But the amounts are unreasonable. And turning those into regular meals is a bad idea. There’s no reason you can’t go keto while eating a hamburger patty or ribeye over a Big Ass Salad. Far more nutrients, far more micronutrients, and it tastes way better.

Eat Less

Maybe if you’re a nomadic horselord sweeping across Europe in the early Bronze Age, you need to eat an entire lamb intestine stuffed with marrow and organs, and you should wash it down with a quart of creamy mare milk. Such a meal would provide the calories you need to see your enemies driven before you and go great with the lamentations of their women. But you’re not a Yamnaya nomad. You’re you.

You probably don’t need that much food, that many calories, and that much fat—since there’s plenty of it on your body already, waiting to be liberated and converted into energy.  Therein lies the beauty of keto. That’s what this is all about: Getting better at burning your own body fat.

Balance Your Fats

The overzealous and protracted drive to demonize all sources of saturated fat as evil has led to a vociferous backlash from the other direction. But just because the supposed experts got the saturated fat issue wrong doesn’t mean the opposite is true: That all the fat we eat should be as saturated as possible.

For one thing, eating nothing but saturated fat is very hard to do using whole foods. Very few animals exist in the world, past or present, with only saturated fat. The only exception I can recall is the coconut, a curious sort of beast that spends most of its time hanging from a tree impersonating a large hairy drupe. Your average slab of beef fat runs about 50% saturated fat, 45% monounsaturated fat, and 5% PUFA. That differs from cut to cut and depending on the diet of the animal, but not by much. It’s similar for other ruminants like bison and lamb. And the most prominent saturated fatty acid in ruminant fat is stearic acid, a fat that converts to monounsaturated oleic acid in the body and has an effect on cholesterol indistinguishable from MUFA or PUFA.

Or take the fatty acid composition of game meat—the type humans encountered and consumed for our entire history.

African kudu (antelope family): 35% SFA, 24% MUFA, 39% PUFA

African impala (antelope family): 51% SFA, 15% MUFA, 33% PUFA

Elk: roughly 40% SFA, 30% MUFA, 30% PUFA

Moose: roughly 33% SFA, 33% MUFA, 33% PUFA

I could go on, but you get the idea: Humans have been consuming a wide range of fatty acids for millennia. It probably makes sense to emulate that intake.

Once again, the folks whose cholesterol goes nuts on keto are outnumbered by those whose cholesterol improves. But if you’re one of the unlucky ones in the former category, try broadening your fatty acid intake (to, ahem, possibly include more nuts):

Focus on monounsaturated fats and fat from meat, rather than isolated sources of saturated fat like butter and coconut oil. You probably don’t have to eliminate those fats. Just don’t make them the centerpiece of your diet.

Eat more avocados, avocado oil, olives, olive oil, and mac nuts for monounsaturated fat. Salads are a great nutrient-dense way to incorporate high-MUFA foods.

Eat more fish. A couple portions of farmed Atlantic salmon were enough to improve LDL-P in overweight men and women. And compared to plain keto, keto + omega-3s from fish has a superior effect on inflammation and metabolic health.

Eat more kudu and impala (if you can get it). Sort of kidding. But really, eat them if you can.

They even have a version of keto called the Spanish ketogenic diet, which features a lot of extra virgin olive oil, olives, fish, and red wine. It works great and might be a good alternative for people whose cholesterol goes wild on saturated fat-heavy keto.

Are Traditional Lipid Markers Even Relevant for Keto Dieters?

Maybe, maybe not.

But be honest about it. You can’t oscillate between championing positive changes to blood lipids on a keto diet and pooh-poohing negative changes to blood lipids on a keto diet.

You can’t use positive changes to prove the efficacy and safety of the ketogenic diet, then turn around and claim that negative changes don’t count because keto dieters are understudied. What if those “positive” changes are actually negative in the context of a ketogenic metabolism? After all, keto dieters are largely understudied in both directions. If what’s unhealthy in a normal dieter might be healthy in a keto dieter, what’s healthy in a normal dieter may be unhealthy in a keto dieter.

I write these things as a strong proponent of spending a significant time in ketosis. As someone who frequently hangs out in a ketogenic state. As someone who wrote a book about keto and is writing another. But also as someone who insists on maintaining strict intellectual honesty and integrity.

We simply don’t know what very high cholesterol numbers mean in the subset of ketogenic dieters who experience them. I strongly suggest not being too flippant about them. 

True: There aren’t any perfect studies examining the utility of conventional cardiovascular risk factors in people eating the type of keto diets you see in the ancestral health space. Maybe your elevated LDL particle number doesn’t mean what it means in the average overweight adult eating the Standard American Diet. Maybe your inflammation is low enough that the risk of atherosclerosis and oxidative modification of LDL is low. But I wouldn’t take that risk, not until we have more data.

What do you think, folks? How did keto affect your blood lipids? Did you make any changes, and if so, did they work? Thanks for stopping in today.

Note: This information isn’t intended as and shouldn’t be considered medical advice. Always consult your doctor in the management or treatment of any health issue.

References:

Hussain TA, Mathew TC, Dashti AA, Asfar S, Al-zaid N, Dashti HM. Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes. Nutrition. 2012;28(10):1016-21.

Phinney SD, Tang AB, Waggoner CR, Tezanos-pinto RG, Davis PA. The transient hypercholesterolemia of major weight loss. Am J Clin Nutr. 1991;53(6):1404-10.

Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metab Clin Exp. 1983;32(8):757-68.

Kleinveld HA, Naber AH, Stalenhoef AF, Demacker PN. Oxidation resistance, oxidation rate, and extent of oxidation of human low-density lipoprotein depend on the ratio of oleic acid content to linoleic acid content: studies in vitamin E deficient subjects. Free Radic Biol Med. 1993;15(3):273-80.

Rosqvist F, Smedman A, Lindmark-månsson H, et al. Potential role of milk fat globule membrane in modulating plasma lipoproteins, gene expression, and cholesterol metabolism in humans: a randomized study. Am J Clin Nutr. 2015;102(1):20-30.

Raatz SK, Johnson LK, Rosenberger TA, Picklo MJ. Twice weekly intake of farmed Atlantic salmon (Salmo salar) positively influences lipoprotein concentration and particle size in overweight men and women. Nutr Res. 2016;36(9):899-906.

De luis D, Domingo JC, Izaola O, Casanueva FF, Bellido D, Sajoux I. Effect of DHA supplementation in a very low-calorie ketogenic diet in the treatment of obesity: a randomized clinical trial. Endocrine. 2016;54(1):111-122.

Pérez-guisado J, Muñoz-serrano A. A pilot study of the Spanish Ketogenic Mediterranean Diet: an effective therapy for the metabolic syndrome. J Med Food. 2011;14(7-8):681-7.

The post Is Keto Bad For Cholesterol? appeared first on Mark's Daily Apple.

[jesseneufeld]

Is Keto Bad For Cholesterol?

We’ve all heard the story. Maybe we’ve even been the protagonist.

Person goes full keto. They lose a bunch of weight, normalize their pre-diabetic glucose numbers, resolve their high blood pressure readings, have more energy, feel great, and have nothing but high praise for the new way of eating.

Except for one thing, everything seems perfect: their cholesterol is sky-high. It throws a wrench into the whole operation, installs a raincloud over the procession, spoils their confidence.

“Could I be killing myself?”

“Are my health improvements just a mirage?”

In other words, are the apparent benefits of keto merely superficial if your cholesterol skyrockets?

The evidence is pretty clear that for the majority of adults who go keto, their cholesterol numbers improve.

In obese adults with type 2 diabetes, a ketogenic diet improved blood lipids and boosted fat loss compared to a low-calorie diet.

In lean, healthy adults without any weight to lose (and who didn’t lose any weight during the course of the diet), total cholesterol went up from 159 to 208 mg/dL and triglycerides fell from 107 to 79 mg/dL. A lipophobic doc might freak out at the rise in TC, but given that the triglycerides dropped, I bet the change reflects a rise in HDL and an overall positive, at worst-neutral effect.

Another study of lean adults with normal cholesterol numbers found that going keto improved their lipids, reducing triglycerides, increasing HDL, and leaving LDL unchanged. Those with small pattern B LDL particles (the “bad kind”) saw their LDL particle size increase, on average. All told, keto was beneficial.

But you aren’t everyone. You aren’t the average of a population. And, given the number of readers I have and the number of people trying a ketogenic diet, there are bound to be some people whose lipid profiles go in the other direction.

I don’t give medical advice here, and I always encourage people to partner with the physicians for health solutions. That said, let me share some thoughts on the keto-cholesterol question….

I’m not just talking about high total cholesterol or high LDL-C. I’m talking about what appears to be the real, legit risk factor for a cardiac event: elevated LDL particle number. According to experts like Dr. Peter Attia and Dr. Chris Masterjohn, atherosclerosis occurs when LDL particles infiltrate the endothelial lining of our arteries. Thus, it’s not high LDL cholesterol that increases the risk of atherosclerosis—LDL-C is the cholesterol found inside the particles— it’s a high number of LDL particles in circulation. The more LDL-P, the greater the chance of them becoming oxidized and infiltrating the arterial wall. There are many factors to consider, like oxidative stress, inflammation, and fatty acid composition of the LDL particles, but all else being equal, a greater number of LDL particles seems to increase the risk of a heart attack.

What Could Be Causing LDL Elevations On Keto?

Weight Loss

I asked Dr. Cate Shanahan for her input on this topic, and she provided a beautiful explanation:

But when you stop eating so many carbs insulin politely steps aside, and your insulin levels plummet. Now your body fat can more easily and more often release its stores of fatty acids into your bloodstream.

When your body fat releases stored fatty acids, any unused fatty acids quickly get picked up by the liver and packed into VLDL lipoprotein. VLDL is a precursor to LDL. So in reducing your insulin levels and increasing your body’s use of fat, you will raise your VLDL, LDL and total cholesterol. You are simply trafficking in fat more often now. And now, because your body stabilizes fat carrying lipoproteins with cholesterol, there is a need for more cholesterol in your blood. These are not bad consequences. They are in fact happy signs your diet is doing what its supposed to be doing.

If you’re actively losing weight, you will probably experience a rise in cholesterol. This is the transient hypercholesterolemia of major weight loss, and it’s a well-known phenomenon. Once your weight stabilizes, cholesterol should normalize—although to a lesser extent than other diets, given Dr. Cate Shanahan’s explanation of increased “trafficking in fat.”

Low Thyroid Function

The thyroid is a barometer for your energy status. If you have plentiful energy to spare, thyroid function is normal. If your body perceives low energy availability, thyroid function may down-regulate. Since the thyroid plays a big role in regulation of LDL receptor activity, its downregulation can lower LDL receptor sites. Fewer LDL-receptors clear LDL particles from the blood. Folks with genetic predispositions to heart disease often have low LDL receptor activity, causing elevated LDL particles. Folks with genetic variants that increase the activity and expression of LDL receptors have lower heart disease rates. Although genes often have different effects that may affect disease risk via other pathways, that’s pretty strong evidence that LDL receptor activity regulates, at least in part, one’s LDL-P and heart disease risk.

Read this post for maintaining thyroid function on keto, and check out Elle Russ’ Paleo Thyroid Solution for an even deeper, more thorough dive into thyroid health.

Eating Too Damn Much

Some keto people pride themselves on gorging. Some are doing it for a good cause—a quest to find the fabled metabolic advantage. Some are doing it to show off and for keto cred—look how much salami I can eat! Some are using keto to deal with unresolved issues with food itself.

Everything I say about doing keto presupposes that you are eating like a normal person. You’re eating as much as you need to fuel your brain and daily activities, fitness and performance goals. You’re leaving the table satiated, not stuffed. For most people, this happens without even trying. It’s why keto is so effective for weight loss.

Genetic Variance

Genes aren’t destiny, but they do modify and regulate our response to a given environmental input.

Some people are dietary cholesterol hyper responders. Unlike the majority of the population, they absorb tons of dietary cholesterol and do not down-regulate their endogenous production to accommodate. The result is an increase in cholesterol synthesis and absorption, leading to a spike in blood cholesterol.

Some people are sensitive to saturated fat. In response to it, they produce elevated numbers of LDL particles. If your keto diet is high in saturated fat and you have a genetic sensitivity to it, your cholesterol will probably skyrocket.

Some people have genes that reduce the activity of their LDL receptors. This will necessarily boost LDL particle numbers.

This topic—genetic variance and how it affects keto—could be an entirely separate post, so I’ll leave it at that (and probably come back to it in the future).

Too Much Butter

Huh? Too much butter, Sisson? Is such a thing even possible?

Maybe. Subjecting cream to the butter-making process strips it of something called milk fat globule membrane (MFGM). And when you compare equal amounts of dairy fat through either cream (with MFGM intact) or butter oil (with MFGM absent), you get very different metabolic effects. Those who ate 40 grams of dairy fat through butter oil saw their lipids worsen, including ApoB, a surrogate for LDL particle number. Those who ate 40 grams of dairy fat through cream saw their lipids unchanged, and in the case of ApoB even improve.  That’s 4 tablespoons of butter compared to 4 ounces, or a half cup, of heavy cream.

Caveats apply here. The subjects weren’t eating a low-carb or ketogenic diet; they just added the butter or cream on top of their normal diet. But in keto people who are genetically susceptible, huge amounts of butter may be responsible for rising LDL-P.

I still love butter. It doesn’t affect my lipids like that. But your mileage may vary, and it’s something to think about if you’re in that situation.

For what it’s worth, whole food dairy like full-fat yogurt, kefir, and cheese do not have the same effect on lipids as butter. They also happen to be keto-friendly and more nutrient-dense.

So, What Can You Do If You See An Increase in LDL?

Start Chugging Soybean Oil

Kidding… It’s true that swapping out some of your animal fats for polyunsaturated seed oils will almost certainly lower your cholesterol levels. It does this by increasing LDL receptor activity, but, being far more unstable than other fats, omega-6 PUFAs also increase the tendency of the LDL particles to oxidize. And since oxidized LDL are the ones that end up wedging in the arterial walls and causing issues, loading up on PUFAs might not be the right path.

You know what just occurred to me? This is an aside, but maybe linoleic acid (the primary fatty acid in seed oils) up-regulates LDL-R activity because the body recognizes the inherent instability of linoleic acid-enriched LDL particles and wants to clear them out before they can cause trouble. I hope some researchers take this idea further.

Stop Being a Keto Caricature.

Half a package of cream cheese for a snack.

Dipping an entire stick of pepperoni into homemade alfredo sauce and calling it dinner.

I’m not saying cream cheese is bad. It’s great. Nor am I suggesting you never eat pepperoni, dipped in alfredo sauce or not. But the amounts are unreasonable. And turning those into regular meals is a bad idea. There’s no reason you can’t go keto while eating a hamburger patty or ribeye over a Big Ass Salad. Far more nutrients, far more micronutrients, and it tastes way better.

Eat Less

Maybe if you’re a nomadic horselord sweeping across Europe in the early Bronze Age, you need to eat an entire lamb intestine stuffed with marrow and organs, and you should wash it down with a quart of creamy mare milk. Such a meal would provide the calories you need to see your enemies driven before you and go great with the lamentations of their women. But you’re not a Yamnaya nomad. You’re you.

You probably don’t need that much food, that many calories, and that much fat—since there’s plenty of it on your body already, waiting to be liberated and converted into energy.  Therein lies the beauty of keto. That’s what this is all about: Getting better at burning your own body fat.

Balance Your Fats

The overzealous and protracted drive to demonize all sources of saturated fat as evil has led to a vociferous backlash from the other direction. But just because the supposed experts got the saturated fat issue wrong doesn’t mean the opposite is true: That all the fat we eat should be as saturated as possible.

For one thing, eating nothing but saturated fat is very hard to do using whole foods. Very few animals exist in the world, past or present, with only saturated fat. The only exception I can recall is the coconut, a curious sort of beast that spends most of its time hanging from a tree impersonating a large hairy drupe. Your average slab of beef fat runs about 50% saturated fat, 45% monounsaturated fat, and 5% PUFA. That differs from cut to cut and depending on the diet of the animal, but not by much. It’s similar for other ruminants like bison and lamb. And the most prominent saturated fatty acid in ruminant fat is stearic acid, a fat that converts to monounsaturated oleic acid in the body and has an effect on cholesterol indistinguishable from MUFA or PUFA.

Or take the fatty acid composition of game meat—the type humans encountered and consumed for our entire history.

African kudu (antelope family): 35% SFA, 24% MUFA, 39% PUFA

African impala (antelope family): 51% SFA, 15% MUFA, 33% PUFA

Elk: roughly 40% SFA, 30% MUFA, 30% PUFA

Moose: roughly 33% SFA, 33% MUFA, 33% PUFA

I could go on, but you get the idea: Humans have been consuming a wide range of fatty acids for millennia. It probably makes sense to emulate that intake.

Once again, the folks whose cholesterol goes nuts on keto are outnumbered by those whose cholesterol improves. But if you’re one of the unlucky ones in the former category, try broadening your fatty acid intake (to, ahem, possibly include more nuts):

Focus on monounsaturated fats and fat from meat, rather than isolated sources of saturated fat like butter and coconut oil. You probably don’t have to eliminate those fats. Just don’t make them the centerpiece of your diet.

Eat more avocados, avocado oil, olives, olive oil, and mac nuts for monounsaturated fat. Salads are a great nutrient-dense way to incorporate high-MUFA foods.

Eat more fish. A couple portions of farmed Atlantic salmon were enough to improve LDL-P in overweight men and women. And compared to plain keto, keto + omega-3s from fish has a superior effect on inflammation and metabolic health.

Eat more kudu and impala (if you can get it). Sort of kidding. But really, eat them if you can.

They even have a version of keto called the Spanish ketogenic diet, which features a lot of extra virgin olive oil, olives, fish, and red wine. It works great and might be a good alternative for people whose cholesterol goes wild on saturated fat-heavy keto.

Are Traditional Lipid Markers Even Relevant for Keto Dieters?

Maybe, maybe not.

But be honest about it. You can’t oscillate between championing positive changes to blood lipids on a keto diet and pooh-poohing negative changes to blood lipids on a keto diet.

You can’t use positive changes to prove the efficacy and safety of the ketogenic diet, then turn around and claim that negative changes don’t count because keto dieters are understudied. What if those “positive” changes are actually negative in the context of a ketogenic metabolism? After all, keto dieters are largely understudied in both directions. If what’s unhealthy in a normal dieter might be healthy in a keto dieter, what’s healthy in a normal dieter may be unhealthy in a keto dieter.

I write these things as a strong proponent of spending a significant time in ketosis. As someone who frequently hangs out in a ketogenic state. As someone who wrote a book about keto and is writing another. But also as someone who insists on maintaining strict intellectual honesty and integrity.

We simply don’t know what very high cholesterol numbers mean in the subset of ketogenic dieters who experience them. I strongly suggest not being too flippant about them. 

True: There aren’t any perfect studies examining the utility of conventional cardiovascular risk factors in people eating the type of keto diets you see in the ancestral health space. Maybe your elevated LDL particle number doesn’t mean what it means in the average overweight adult eating the Standard American Diet. Maybe your inflammation is low enough that the risk of atherosclerosis and oxidative modification of LDL is low. But I wouldn’t take that risk, not until we have more data.

What do you think, folks? How did keto affect your blood lipids? Did you make any changes, and if so, did they work? Thanks for stopping in today.

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Note: This information isn’t intended as and shouldn’t be considered medical advice. Always consult your doctor in the management or treatment of any health issue.

References:

Hussain TA, Mathew TC, Dashti AA, Asfar S, Al-zaid N, Dashti HM. Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes. Nutrition. 2012;28(10):1016-21.

Phinney SD, Tang AB, Waggoner CR, Tezanos-pinto RG, Davis PA. The transient hypercholesterolemia of major weight loss. Am J Clin Nutr. 1991;53(6):1404-10.

Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metab Clin Exp. 1983;32(8):757-68.

Kleinveld HA, Naber AH, Stalenhoef AF, Demacker PN. Oxidation resistance, oxidation rate, and extent of oxidation of human low-density lipoprotein depend on the ratio of oleic acid content to linoleic acid content: studies in vitamin E deficient subjects. Free Radic Biol Med. 1993;15(3):273-80.

Rosqvist F, Smedman A, Lindmark-månsson H, et al. Potential role of milk fat globule membrane in modulating plasma lipoproteins, gene expression, and cholesterol metabolism in humans: a randomized study. Am J Clin Nutr. 2015;102(1):20-30.

Raatz SK, Johnson LK, Rosenberger TA, Picklo MJ. Twice weekly intake of farmed Atlantic salmon (Salmo salar) positively influences lipoprotein concentration and particle size in overweight men and women. Nutr Res. 2016;36(9):899-906.

De luis D, Domingo JC, Izaola O, Casanueva FF, Bellido D, Sajoux I. Effect of DHA supplementation in a very low-calorie ketogenic diet in the treatment of obesity: a randomized clinical trial. Endocrine. 2016;54(1):111-122.

Pérez-guisado J, Muñoz-serrano A. A pilot study of the Spanish Ketogenic Mediterranean Diet: an effective therapy for the metabolic syndrome. J Med Food. 2011;14(7-8):681-7.

The post Is Keto Bad For Cholesterol? appeared first on Mark's Daily Apple.

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