Is Glucose An Amino Acid?

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Is Glucose An Amino Acid?

Amino acids are the monomers that combine to make peptides and proteins. Amino acids have an amine group (NHtext2) at one end of the molecule and a carboxyl group (COOH) on the other end. Get access to this video and our entire Q&A library from General Studies Health Science: Help & Review Become a member and unlock all StudyAnswers Explore our homework questions and answer library Ask a study question and one of our experts will send you an answer within hours. By submitting, I am agreeing to the Terms of Use and Honor Code To ask a site support question, click here When your answer is ready, it will appear on your Dashboard . New! Get a text message when your answer is ready Thanks! We'll text you when your answer is ready! Receive an email or text message when your answer is ready to view Email already in use. Already a member? Log In instead. We will send you an email and/or text message when you answer is ready. Thanks! We'll notify you when your answer is ready! Your notification info was successfully sent. Study.com's video lessons can help you master all major subjects Create your account. No obligation; cancelanytime. Start your FREE trial. No obligation; cancelanytime. E Continue reading >>

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  1. tim

    Firstly I want to preface with the fact that I'm not arguing as to the effects of saturated fats on your body and the many potential misconceptions the health industry has about saturated fats, I'm simply attempting identify a method of reaching ketosis through diet that can be achieved by anyone, consistently, without raising LDL cholesterol levels regardless of fitness levels and activity. Many people are scared off the diet after receiving blood work because of increased LDL and the more blood tests like these are seen by medical professionals the more it proliferates the negative opinions of ketogenic diets amongst the medical community.
    I made a post
    34 to the Facebook group today regarding the results of clinical studies vs individual reports of elevations in LDL cholesterol after following a ketogenic diet periods of up to 6-12 months. I'm creating this topic as a means for me to follow up on my blood panels over the coming weeks and to further break down my reasoning behind what I'm doing.
    Objective: Identifying a method of reaching ketosis consistently (through diet only) without increasing LDL cholesterol levels regardless of activity level by adapting saturated vs unsaturated fat intake to individual variables.
    Clinical studies have shown that ketogenic diets high in polyunsaturated fats result in increased ketone levels when compared to diets high in saturated fats. Additionally, the diets high in polyunsaturated fats resulted in no adverse effects on LDL cholesterol levels, while the diets higher in saturated fats resulted in significant increases.
    Link to full article
    Differential metabolic effects of saturated versus polyunsaturated fats in ketogenic diets.
    BS Fuehrlein, MS Rutenberg, JN Silver, MW Warren, DW Theriaque, GE Duncan, PW Stacpoole and ML Brantly, The Journal of clinical endocrinology and metabolism, Apr 2004
    Ketogenic diets (KDs) are used for treatment of refractory epilepsy and metabolic disorders. The classic saturated fatty acid-enriched (SAT) KD has a fat:carbohydrate plus protein ratio of 4:1, in which the predominant fats are saturated. We hypothesized that a polyunsaturated fat-enriched (POLY) KD would induce a similar degree of ketosis with less detrimental effects on carbohydrate and lipid metabolism. Twenty healthy adults were randomized to two different weight-maintaining KDs for 5 d. Diets were 70% fat, 15% carbohydrate, and 15% protein. The fat contents were 60 or 15% saturated, 15 or 60% polyunsaturated, and 25% monounsaturated for SAT and POLY, respectively. Changes in serum beta-hydroxybutyrate, insulin sensitivity (S(I)), and lipid profiles were measured. Mean circulating beta-hydroxybutyrate levels increased 8.4 mg/dl in the POLY group (P = 0.0004), compared with 3.1 mg/dl in the SAT group (P = 0.07). S(I) increased significantly in the POLY group (P = 0.02), whereas total and low-density lipoprotein cholesterol increased significantly in the SAT group (both P = 0.002). These data demonstrate that a short-term POLY KD induces a greater level of ketosis and improves S(I), without adversely affecting total and low-density lipoprotein cholesterol, compared with a traditional SAT KD. Thus, a POLY KD may be superior to a classical SAT KD for chronic administration.
    There are many arguments about whether or not having higher levels of LDL cholesterol matters as much as the medical community at large says it does but the fact remains, most medical professionals consider high levels of LDL to be dangerous and will recommend people stop the ketogenic diet more often than not.
    This causes two immediate problems:
    The individual panics and their first reaction is to stop the diet immediately, at the very least they'll continue amidst healthy anxiety
    The results of the blood test proliferate the stigma amongst medical professionals that there is causation between ALL ketogenic diets and higher levels of LDL cholesterol regardless of what the diet constituted of
    But some people have reductions in LDL cholesterol while on a high saturated fat versions of the keto diet, how can you explain that?
    While definitely not the only factor, the most obvious factor could be the level of physical activity the individual is involved in and the TYPE of physical activity it is. Studies have shown that aerobic exercise prevents increases in cholesterol from diets high in saturated fat.
    Increased blood cholesterol after a high saturated fat diet is prevented by aerobic exercise training.
    JF Ortega, VE Fernández-Elías, N Hamouti and R Mora-Rodriguez, Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme, Jan 2013
    A high saturated fatty acids diet (HSFAD) deteriorates metabolic and cardiovascular health while aerobic training improves them. The aim of this study was to investigate in physically inactive and overweight people if 2 weeks of HSFAD leads to hyperlipemia or insulin resistance and if concurrent aerobic exercise training counteracts those effects. Fourteen overweight (body mass index, 27.5 ± 0.6 kg·m(-2)), healthy, young individuals (aged 24.8 ± 1.8 years) were randomly assigned to a diet (D) or a diet plus exercise (D + E) group. During 14 consecutive days both groups increased dietary saturated fatty acids from 31 ± 10 to 52 ± 14 g·day(-1) (p < 0.001) while maintaining total fat intake. Concurrent to the diet, the D + E group underwent 11 cycle-ergometer sessions of 55 min at 60% peak oxygen uptake (V˙O(2peak)). Before and after intervention, insulin sensitivity and body composition were estimated, and blood lipids, resting blood pressure, and VO(2peak) were measured. Body weight and composition, plasma free fatty acids composition and concentration, and insulin sensitivity remained unchanged in both groups. However, post-intervention total cholesterol (T(C)) and low-density lipoprotein cholesterol (LDL-C) increased above pre-intervention values in the D group (147 ± 8 to 161 ± 9 mg·dL(-1), p = 0.018 and 71 ± 10 to 82 ± 10 mg·dL(-1), p = 0.034, respectively). In contrast, in the D + E group, T(C) and LDL-C remained unchanged (153 ± 20 to 157 ± 24 mg·dL(-1) and 71 ± 21 to 70 ± 25 mg·dL(-1)). Additionally, the D + E group lowered systolic blood pressure (6 ± 2 mm Hg, p = 0.029) and increased VO(2peak) (6 ± 2 mL·kg(-1)·min(-1), p = 0.020). Increases in T(C) and LDL-C concentration induced by 14 days of HSFAD can be prevented by concurrent aerobic exercise training, which, in addition, improves cardiorespiratory fitness.
    The ketogenic diet is gaining immense traction however it still suffers from one major setback, reports of increases in LDL cholesterol and the inevitable stigma that follows. To combat this stigma we now have research that shows our preconceptions of LDL may be unfounded to a certain degree, but like anything these arguments will take a long time to become mainstream.
    While there are many people that have successfully transitioned to a ketogenic diet without taking saturated vs unsaturated fats into consideration (and that's great for them) and have perfect blood work there are many that haven't. Instead of treating ketogenic diets as a one-size-fits-all approach backed up with modern & fringe arguments about LDL levels I propose that more thought needs to be put into the induction process.
    Before starting a ketogenic diet some questions need to be asked, these are just a few basic ideas that I've thrown around based on the studies I've read and sifting through causation and correlations.
    What is your level of activity? If you are very active aerobically then increasing your intake of saturated fats won't have the same impact on your LDL levels that someone with a sedentary lifestyle has (although the amount may differ for the individual). The goal, of course, is for everyone to be active but there are many heavy people on a ketogenic diet that are unable to exercise at their current weight. In these cases recommending at least a 20/80 ratio of saturated vs unsaturated fats may be a better approach until activity levels can be increased.
    Will elevations in LDL put you off the diet? GP's well versed in ketogenic diets are few and far between and you can't throw a stone without hitting a story about someone's GP recommending they stop their diet immediately 6 months into their diet. If this is something that will prevent you from continuing with your diet then reducing saturated fats may be a way of sticking to the diet long term while showing your GP that ketogenic diets can help lower LDL cholesterol at the same time leading them to become more interested in the topic and not writing it off. On the other hand if you are confident in studies regarding LDL not being as bad as previously thought then this won't be as much of an issue for you.
    There are still some unanswered questions that I hope to find the answers to, for instance how do the effects of cholesterol mobilising due to weight loss combat the effects of reducing saturated fat intake? Will one outweigh the other and if so which?

    I'll follow up with my own blood work and other results over the next several weeks.

  2. BillJay

    Great thread, I'll be watching since my LDL is sky-high and although it is Pattern A and currently considered to be unlikely to contribute to atherogenicity, the science is always evolving and that might change.

    Clinical studies have shown that ketogenic diets high in polyunsaturated fats result in increased ketone levels when compared to diets high in saturated fats.
    I want to point out that in the following YouTube video Dr. Cate Shanahan points out the mechanism by which polyunsaturated fats work to lower LDL, which is why they're recommended by mainstream medical dogma, is to cause the LDL to actually stick to the vascular linings which induces atherogenic plaque, so it's usually a choice between saturated and monounsaturated fat while polyunsaturated fats should be incidental to the other fats consumed and not the determining factor.
    YouTube: Dr. Cate Shanahan - 'Practical Lipid Management for LCHF Patients'
    Dr. Cate Shanahan - 'Practical Lipid Management for LCHF Patients'

    (The YouTube link in the editor appears fine, but when saved, it doesn't display correctly, so I'll monitor this and update it as necessary.)

  3. larry

    I'm bookmarking this fascinating and important thread.

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