Hey everyone,

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I've been on the keto diet for the past three months. I started the diet because I was frustrated with my hip size, and despite training at the gym and eating healthy food for the last year, I didn't see any improvement, except my arms became bigger. I wanted to reduce the swelling in my hips, so I decided to try the keto diet since everyone was praising it.

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Surprisingly, I noticed a difference in my hip size in less than two weeks. I was thrilled with the results, so I continued with the diet. I've lost 45 pounds in the past three months and feel great. My energy levels are high, and I'm no longer experiencing bloating or stomach discomfort.

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I feel better than ever, and the best part is that I enjoy everything I eat and don't feel hungry anymore. It might be thanks to choosing veggie powders from a natural foods company instead of fresh vegetables that always made my gut uncomfortable. Still, something tells me it's because I didn't have to give up fatty food as I did before with other diets.

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However, I've been reading a lot about the long-term safety of the keto diet, and I'm starting to worry. I've seen conflicting information online, some saying it's perfectly safe to follow the keto diet long-term, while others say it's not safe to eat this way for an extended period.

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I'm hesitant to stop the diet because I've seen such exceptional results, but I'm also worried about the potential health risks associated with following the diet for too long. I've heard about the potential for kidney damage, nutrient deficiencies, and other health problems.

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I hope I can find some answers here. What is the maximal term you have followed such an eating plan, and have you experienced any negative side effects? Are there any statistics on this?

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I'd love to hear your thoughts and advice on this. Thank you in advance!

Like many others, I’ve always wondered what it is that makes some people able to get away with being able to eat whatever they want and remain lean and/or without underlying poor health. After having made the switch low carb living (and more recently zero carb) some time ago I also began to specifically wonder what makes people more or less sensitive to dietary carbohydrate intake than others.

This paragraph here from the r/zerocarb sub wiki describes the nuances in carbohydrate tolerance within humans that I’ve wondered about.

the 'people who can eat anything and remain lean', the people who find effortless maintenance when they cut out soda and most sugar but still include grains and starches, the people who need to be low carb (no sugar or starches, around 50g of low glycemic carbs), the very low carb ketogenic (sub 20g), and the zerocarbers.

I made a quite rapid descent thru all of these dietary archetypes before finally realizing my status as a someone who needs to be a zerocarber for optimal health.

Before being introduced to the concept of removing carbohydrate from my diet, I tried existing in the ‘people who find effortless maintenance when they cut out soda and most sugar but still include grains and starches’ category for some time because that’s what’s currently pushed as the gold standard for healthy diet. Don’t completely cut out carbs, just the refined ones. Sometimes this way of eating is referred to as a ‘low glycemic’ diet. If carbs are going to be consumed, they should be ones that are unrefined snd don’t have as much of an impact on blood glucose. So things like quinoa and bulgur wheat instead of rice, wholegrain bread instead of white bread, sweet potato instead of white potato, lots of fibrous veggies.

This method of eating ultimately ended up not working for me as it was not effortless to maintain health with, in the way that it’s effortless for me to maintain health by completely omitting carbs from my diet. Trying to eat a low glycemic diet left me nearly as hungry as I was when I was eating a diet heavy in refined and unrefined carbohydrate food sources. I’d also tried a normal ketogenic diet which improved satiety and appetite regulation, but again health maintenance and appetite regulation on keto was not as effortless as it has been on zerocarb.

Part of me wants to chalk this up to me having Polycystic Ovarian Syndrome, an inherited, chronic metabolic disorder that predisposes me to carb sensitivity. This makes me wonder if all of us for whom a diet devoid of carbohydrate is what’s needed for optimal health all have inherited metabolic disorders that make us predisposed to carbohydrate intolerance.

But then what about those who do not have any sort of genetic/inherited chronic metabolic disorder who still ultimately find it impossible to maintain health without removing carbohydrate from their diet? What’s the difference between such people, and people who also do not have metabolic disorders but find themselves being able to eat as much carbohydrate as they want without compromising their health? (So again to reiterate we have two groups of people Group A— people who do not have inherited metabolic disorders that predispose them to carbohydrate intolerance but still find it necessary to remove carbs from their diet to maintain health and Group B—people who do not have inherited metabolic disorders and don’t find it necessary to cut carbs from their diet to maintain health)

The only information I’ve found that can even begin to give me some sort of answer to this question is information about the AMY1 gene (produces salivary amylase, an enzyme that aids in the digestion of carbohydrate) and how some people have more copies of this gene than others, making carbohydrate metabolism easier for those who have more copies and harder for those who have less.

Is that all it really comes down to in people who don’t have metabolic disorders that predispose them to carbohydrate intolerance? Just a difference in the amount of AMY1 gene copies they possess?

Am hoping to get recommendations for protein powder or collagen. I've tried at least 10 highly rated versions and all of them gave me extreme anxiety.

Hoping nutrition experts might have some advise. Not super knowledgeable about how to deal with this situation.

Thanks so much

Orthopaedic surgeon Dr Gary Fettke, was sanctioned by his medical board for suggesting low sugar diets to his diabetic patients.

Fettke’s belief in the importance of preventative medicine has triggered his lifelong research into the science of nutrition, dietary guidelines and exactly what makes a healthy diet.

And he has become convinced that for all of us - not just those with diabetes - sugar, refined carbs and polyunsaturated fats come together to create the perfect storm in our bodies. That is what, he believes, is driving higher levels of metabolic illnesses - such as diabetes type 2, heart disease and cancer - than we have ever seen before. And he reveals the dietary changes you can make to minimise the risk of these diseases.

You can listen to the podcast on:

Apple or Spotify

And here's a bit about me:

The podcast is hosted by me, Liz Tucker. It's aimed at both medical professionals and patients. Here are my credentials: I am an award winning medical journalist who made films for many years for the BBC. My documentaries have been shown in over 100 countries.

If you'd like to see more about my credentials, here's a link to the website:

Podcast Website

Many thanks

Liz

New Findings:

• What is the central question of the study?
  Can a novel, energy-dense and lightweight ketogenic bar (1000 kcal) consumed 3 h before exercise modulate steady-state incline rucksack march (‘ruck’) performance compared to isocaloric carbohydrate bars in recreationally active, college-aged men?

• What is the main finding and its importance?
  Acute ingestion of either nutritional bar sustained ∼1 h of exhaustive rucking with a 30% of body weight rucksack. This proof-of-concept study is the first to demonstrate that carbohydrate bars and lipid bars are equally feasible for preserving ruck performance. Novel ketogenic nutrition bars may have military-relevant applications to lessen carry load without compromising exercise capacity.

Abstract:

Rucksack marches (‘rucks’) are strenuous, military-relevant exercises that may benefit from pre-event fueling. The purpose of this investigation was to explore whether acute ingestion of carbohydrate- or lipid-based nutritional bars before rucking can elicit unique advantages that augment exercise performance. Recreationally active and healthy males (n = 29) were randomized and counterbalanced to consume 1000 kcal derived from a novel, energy-dense (percentage energy from carbohydrate/fat/protein: 5/83/12) ketogenic bar (KB), or isocaloric high-carbohydrate bars (CB; 61/23/16) 3 h before a time-to-exhaustion (TTE) ruck. Conditions were separated by a 1-week washout. The rucksack weight was standardized to 30% of bodyweight. Steady-state treadmill pace was set at 3.2 km/h (0.89 m/s) and 14% grade. TTE was the primary outcome; respiratory exchange ratio (RER), capillary ketones (R-β-hydroxybutyrate), glucose and lactate, plus subjective thirst/hunger were the secondary outcomes. Mean TTE was similar between conditions (KB: 55 ± 25 vs. CB: 54 ± 22 min; P = 0.687). The RER and substrate oxidation rates revealed greater fat and carbohydrate oxidation after the KB and CB, respectively (all P < 0.0001). Capillary R-βHB increased modestly after the KB ingestion (P < 0.0001). Neither bar influenced glycaemia. Lactate increased during the ruck independent of the condition (P < 0.0001). Thirst/fullness perceptions changed independent of the nutritional bar consumed. A novel KB nutritional bar produced equivalent TTE ruck results to the isocaloric CBs. The KB's energy density relative to CB (6.6 vs. 3.8 kcal/g) may provide a lightweight (–42% weight), pre-event fueling alternative that does not compromise ruck physical performance.

Full-text Link and Authors:

https://physoc.onlinelibrary.wiley.com/doi/full/10.1113/EP091029

Alex Buga, Chris D. Crabtree, Justen T. Stoner, Drew D. Decker, Bradley T. Robinson, Madison L. Kackley, Teryn N. Sapper, Jeffrey D. Buxton, Dominic P. D'Agostino, Tyler S. McClure, Anthony Berardi, Shawn Cline, Trevor Fleck, Jared Krout, Doran Newby, Andrew P. Koutnik, Jeff S. Volek, Philip J. Prins*

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Figure 1 - Study Design

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Figure 2 - Experimental Timeline

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Figure 3 - Performance Results

I am currently trying a ketogenic diet with the purpose of improving on my cognitive deficits following a head injury. The main reason that encouraged me to select it as my option can not only be attributed to the consensus on it being a net positive for other neurological conditions but also a specific phenomenon I will get into.

So whenever I try to "think" with the injured region I begin breathing heavily. The point I amt rying to make is that since oxygenization is used so an initial cellular metabolism can be triggered and as a result enablw the use of glucose reverses, then that means my brain cell engines have issues being able to perform said process (hence brain fog)

This has led me to wonder, if providing ketones as an alternate source would mean less energy expenditure is required, then the ability of the mitochondria to fully function on itself wouldnt compromise the overall status of my cognition.

Does anyone have articles detailing the full process?

I use a keto diet to manage my prediabetes but my primary diagnosis is Crohn's Disease. This last year, I relied heavily on stevia and sucralose. However my gastroenterologist has told me that I need to avoid them (along with all sugar and natural sweeteners). The only rationale that I can find for this is that artificial sweeteners have affected the microbiome of mice/rats when given in large quantities. I cannot tolerate some sweeteners like sugar alcohols. I am wondering if I am really wrecking my health by sticking with stevia and Splenda. Any ideas about this? Research that you have heard about?

https://www.npr.org/2023/03/06/1161225855/diabetes-obesity-rising-study-young-adults

~sigh. While this is a lay overview, the science isn't there. It's mostly a repeat of the establishment view and zero understanding of how carbs impact diabetes/obesity.

Latest work from cancer research specialist, Dr Thomas Seyfried.

https://www.biorxiv.org/content/10.1101/2022.12.01.518661v1

From Twitter: "Our new study shows that OxPhos is not needed for the viability of cultured breast and liver tumor cells making oxygen consumption an ambiguous marker for ATP synthesis through OxPhos."

Comment from Dr Richard Cheng: "Tom, Does this nullify some of the arguments that cancer cells can burn fat as fuel?"

Reply from Dr Seyfried: "Yes. We have not yet found a cancer cell that can survive on fatty acids or ketone bodies alone or in the absence of glucose or glutamine, which are fermented for energy. Fatty acids cannot be fermented!"

Cancer loves sugar and can't thrive on fatty acids or ketones for energy. Otto Warburg discovered way back in the 1930s that cancer thrives on sugar irrespective of whether there is oxygen present or not. He was a homosexual Jew who worked on cancer research with Hitler's protection, despite the fact that other Jews and homosexuals were targeted by Hitler. He lived in a luxury estate granted by Hitler, with horses to ride, while other Jews perished. Consequently he was despised, and after the war his work was ignored, which was too bad for the millions of people who were to get cancer over the next several decades. [His story is described in the book Ravenous by Sam Apple.]

In recent years, the Metabolic Theory of cancer has been taken up by such doctors as Thomas Seyfried. [Interestingly, there is a parallel movement starting up in psychiatry. Chris Palmer's book Brain Energy describes this.]

I would love to hear this sub's opinion about this recent Erythritol study published on Feb 27th, 2023 in Nature.

Title:

The artificial sweetener erythritol and cardiovascular event risk

Authors:

Marco Witkowski et. al.

Abstract:

Artificial sweeteners are widely used sugar substitutes, but little is known about their long-term effects on cardiometabolic disease risks. Here we examined the commonly used sugar substitute erythritol and atherothrombotic disease risk. In initial untargeted metabolomics studies in patients undergoing cardiac risk assessment (n = 1,157; discovery cohort, NCT00590200), circulating levels of multiple polyol sweeteners, especially erythritol, were associated with incident (3 year) risk for major adverse cardiovascular events (MACE; includes death or nonfatal myocardial infarction or stroke). Subsequent targeted metabolomics analyses in independent US (n = 2,149, NCT00590200) and European (n = 833, DRKS00020915) validation cohorts of stable patients undergoing elective cardiac evaluation confirmed this association (fourth versus first quartile adjusted hazard ratio (95% confidence interval), 1.80 (1.18–2.77) and 2.21 (1.20–4.07), respectively). At physiological levels, erythritol enhanced platelet reactivity in vitro and thrombosis formation in vivo. Finally, in a prospective pilot intervention study (NCT04731363), erythritol ingestion in healthy volunteers (n = 8) induced marked and sustained (>2 d) increases in plasma erythritol levels well above thresholds associated with heightened platelet reactivity and thrombosis potential in in vitro and in vivo studies. Our findings reveal that erythritol is both associated with incident MACE risk and fosters enhanced thrombosis. Studies assessing the long-term safety of erythritol are warranted.

Link to study:

https://www.nature.com/articles/s41591-023-02223-9.epdf?sharing_token=k-Rcy1AI_47QDaN4IYrv2tRgN0jAjWel9jnR3ZoTv0MTnVt_Yzm2YDkmKtSZJOysYZlROr0ymfAdj9yPHH8bMVWpKjhPzPeMT8zTG9DpNMmnfRfOqNqOH8PhwI2X9sxfHMa-Tpawl-dyIWq9WdTUO2lqDJWIHLoFK3aG5AGi1Yg1zHmeYpNKpcP0rJEwRuXM-UwQ_iUx2TdtuE39badalw%3D%3D&tracking_referrer=www.cnn.com

Hi. very interested in any anecdotal or otherwise evidence that after 2 stents 2 years ago I have basically been living in Ketosis for over 3-4 years, previous smoker etc before heart attack etc but very fit 2.1klms swim and 30 minute spin bike 5 days per week. My doctor once again rand and gave me a serve about my ketosisis lifestyle saying as usual" I am being very stupid " their is no reason trying to assuage his beliefs thats what they learn but it did make me question once again, that I am doing the right thing. Generally bloods are all good cholesterol at higher end of normal range. I take aspirin,statin & blood pressure meds, stopped the beta blocker. I also take magnesium, vitamin A, multi vitamin and iron. Just looking for reasons to listen to the Dr, lol I enjoy my ketosis lifestyle and would like to keep it. Only reason I take the blood pressure med and statin and aspirin is to keep the Dr. happy and family, I would prefer to take zero.

We all know that heat extracted industrial seed/bean oils are bad, and cold pressed fruit oils like olive, avocado and coconut are good. Where does peanut oil fit in?

https://www.frontiersin.org/articles/10.3389/fnut.2023.1084021/full

Authors (impressive list):

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https://preview.redd.it/k8cthffe96ha1.png?width=824&format=png&auto=webp&v=enabled&s=bbe03a6b2d7a9c2b472afb0cb92474bfbd8aa7e8

Abstract

High carbohydrate, low fat (HCLF) diets have been the predominant nutrition strategy for athletic performance, but recent evidence following multi-week habituation has challenged the superiority of HCLF over low carbohydrate, high fat (LCHF) diets, along with growing interest in the potential health and disease implications of dietary choice. Highly trained competitive middle-aged athletes underwent two 31-day isocaloric diets (HCLF or LCHF) in a randomized, counterbalanced, and crossover design while controlling calories and training load. Performance, body composition, substrate oxidation, cardiometabolic, and 31-day minute-by-minute glucose (CGM) biomarkers were assessed.

We demonstrated:

1. equivalent high-intensity performance (@∼85%VO2max), fasting insulin, hsCRP, and HbA1c without significant body composition changes across groups;
2. record high peak fat oxidation rates (LCHF:1.58 ± 0.33g/min @ 86.40 ± 6.24%VO2max; 30% subjects > 1.85 g/min);
3. higher total, LDL, and HDL cholesterol on LCHF;
4. reduced glucose mean/median and variability on LCHF.

We also found that the 31-day mean glucose on HCLF predicted 31-day glucose reductions on LCHF, and the 31-day glucose reduction on LCHF predicted LCHF peak fat oxidation rates. Interestingly, 30% of athletes had 31-day mean, median and fasting glucose > 100 mg/dL on HCLF (range: 111.68-115.19 mg/dL; consistent with pre-diabetes), also had the largest glycemic and fat oxidation response to carbohydrate restriction. These results: (i) challenge whether higher carbohydrate intake is superior for athletic performance, even during shorter-duration, higher-intensity exercise; (ii) demonstrate that lower carbohydrate intake may be a therapeutic strategy to independently improve glycemic control, particularly in those at risk for diabetes; (iii) demonstrate a unique relationship between continuous glycemic parameters and systemic metabolism.

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https://doi.org/10.1111/jsr.13832

https://pubmed.ncbi.nlm.nih.gov/36734405

Abstract

Extended wakefulness, or sleep deprivation, impairs cognitive performance and brain glucose metabolism. A ketogenic diet (KD) provides an alternative fuel source, ketone bodies, that could elicit a metabolic benefit during sleep deprivation. A randomised, cross-over trial was conducted with seven male military personnel. Participants ingested an iso-energetic ketogenic diet or carbohydrate-based diet for 14 days, immediately followed by 36 h of extended wakefulness and separated by a 12 day washout. Cognitive performance, mood, subjective sleepiness, capillary blood glucose, and D-β-hydroxybutyrate concentrations were measured every 2 h during extended wakefulness. Linear mixed models were used to analyse data. D-β-hydroxybutyrate was higher (p < 0.001) and glucose was lower (p < 0.01) on the KD compared with the carbohydrate-based diet. The KD improved psychomotor vigilance task performance (number of lapses, mean reciprocal response time, mean fastest 10% response time (RT), and mean slowest 10% RT, all p < 0.05), running memory continuous performance test performance (RT and number of correct responses per minute, both p < 0.01), and vigour, fatigue, and sleepiness (all, p ≤ 0.001) compared with the carbohydrate-based diet. In conclusion, a KD demonstrated beneficial effects on cognitive performance, mood, and sleepiness during 36 h of extended wakefulness compared with a carbohydrate-based diet.

Authors:

• Henderson LR
• van den Berg M
• Shaw DM

------------------------------------------ Info ------------------------------------------

Open Access: True

Additional links: * https://doi.org/10.1111/jsr.13832

https://www.mdpi.com/2072-6643/15/4/825

Abstract

Very low-calorie ketogenic diets (VLCKD) are widely employed in successful weight-loss strategies. Herein, we evaluated the efficacy and safety of a VLCKD on non-alcoholic fatty liver disease (NAFLD) and parameters commonly associated with this condition in overweight and obese subjects who did not take any drugs. This prospective, real-life study included thirty-three participants who followed a VLCKD for 8 weeks. NAFLD was diagnosed using transient elastography (FibroScan). Data on anthropometric measurements, bioimpedance analysis, and biochemical assays were gathered both before and after the dietary intervention. BMI (kg/m2) (from 33.84 ± 6.55 to 30.89 ± 6.38, p < 0.01), waist circumference (cm) (from 106.67 ± 15.51 to 98.64 ± 16.21, p < 0.01), and fat mass (Kg) (from 38.47 ± 12.59 to 30.98 ± 12.39, p < 0.01) were significantly lower after VLCKD. CAP (db/m), the FibroScan parameter quantifying fatty liver accumulation, showed a significant reduction after VLCKD (from 266.61 ± 67.96 to 223 ± 64.19, p < 0.01). After VLCKD, the fatty liver index (FLI), a benchmark of steatosis, also revealed a significant decline (from 62.82 ± 27.46 to 44.09 ± 31.24, p < 0.01). Moreover, fasting blood glucose, insulin, triglycerides, total cholesterol, LDL-cholesterol, ALT, γGT, and FT3 blood concentrations, as well as insulin resistance (quantified by HOMAIR) and systolic and diastolic blood pressure levels, were significantly lower after VLCKD (p < 0.01 for all the parameters). By contrast, HDL-cholesterol, 25 (OH) vitamin D, and FT4 blood concentrations were higher after VLCKD (p < 0.01 for all parameters). The variation (δ) of CAP after VLCKD did not show a correlation with the δ of any other parameter investigated in this study. We conclude that VLCKD is a helpful approach for NAFLD independent of changes in factors commonly associated with NAFLD (obesity, fat mass, insulin resistance, lipids, and blood pressure) as well as vitamin D and thyroid hormone levels.

https://www.mdpi.com/1422-0067/24/4/3102

Abstract

The ketogenic diet (KD), a diet high in fat and protein but low in carbohydrates, is gaining much interest due to its positive effects, especially in neurodegenerative diseases. Beta-hydroxybutyrate (BHB), the major ketone body produced during the carbohydrate deprivation that occurs in KD, is assumed to have neuroprotective effects, although the molecular mechanisms responsible for these effects are still unclear. Microglial cell activation plays a key role in the development of neurodegenerative diseases, resulting in the production of several proinflammatory secondary metabolites. The following study aimed to investigate the mechanisms by which BHB determines the activation processes of BV2 microglial cells, such as polarization, cell migration and expression of pro- and anti-inflammatory cytokines, in the absence or in the presence of lipopolysaccharide (LPS) as a proinflammatory stimulus. The results showed that BHB has a neuroprotective effect in BV2 cells, inducing both microglial polarization towards an M2 anti-inflammatory phenotype and reducing migratory capacity following LPS stimulation. Furthermore, BHB significantly reduced expression levels of the proinflammatory cytokine IL-17 and increased levels of the anti-inflammatory cytokine IL-10. From this study, it can be concluded that BHB, and consequently the KD, has a fundamental role in neuroprotection and prevention in neurodegenerative diseases, presenting new therapeutic targets.

https://www.cell.com/heliyon/fulltext/S2405-8440(23)00653-900653-9)

Abstract

Medium-chain triglycerides (MCT) possess neuroprotective properties. However, the long-term metabolic consequences of supplementing a regular diet with cognition-enhancing doses of MCT are largely unknown. We studied the effects of chronic (28 days) supplementation of regular diet with different doses of MCT oil (1, 3, or 6 g/kg/day) or water (control) on working memory (Y-maze), behavior in the Open Field, spatial learning (Morris water maze), and weight of internal organs in male Wistar 2.5-m.o. Rats. In a separate experiment, we evaluated acute (single gavage) and chronic (28 days) effects of MCT or lard supplementation (3 g/kg) on blood biochemical parameters. MCT-1 and MCT-3 doses improved working memory in YM. In MWM, MCT-6 treatment improved spatial memory. Chronic MCT-1 or MCT-3 treatment did not affect internal organ weight, while MCT-6 dose increased liver weight and the brown/white adipose tissue ratio. Acutely, MCT administration elevated blood β-hydroxybutyrate and malondialdehyde levels. Chronic MCT administration (3 g/kg) did not affect the blood levels of glucose, lactate, pyruvate, acetoacetate, β-hydroxybutyrate, total and HDL cholesterol, triglycerides, malondialdehyde, and aspartate transaminase and alanine transaminase activities. Therefore, daily supplementation of standard feed with MCT resulted in mild intermittent ketosis. It improved working memory at lower concentrations without significant adverse side effects. At higher concentrations, it improved long-term spatial memory but also resulted in organ weight changes and is likely unsafe. These results highlight the importance of monitoring the metabolic effects of MCT supplementation alongside cognitive assessment in future studies of MCT's neuroprotective properties.

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