Daniel T

· Is there a threshold for blood sugar that when kept below does no harm, and when above does? All animal life, unless it is a bloodless alien, will raise their blood sugars if sugar, or sugar forming starches, are eaten. Eating rice or potatoes will, specifically and especially, raise blood sugar. The question then becomes, is the amount of elevation and accumulation of glucose in the bloodstream harmful? The crux of the ‘safe starches’ argument is that no harm will come of this and it is, in fact, healthy. It is acknowledged that blood glucose will elevate after eating ‘safe starches’, but will generally stay below 140 mg/dl that Jaminet says is perfectly safe. Is it?? The science writing (below) is on the wall and the answer is…clearly no. It is important to realize that this answer is no; there is no safe intake of sugar, nor a threshold level of blood sugar below which no harm will come, and I will shortly devote a fair amount of time to show this. It is also comforting to hear Jaminet and others say that perhaps while some people cannot tolerate spikes in glucose, most people can. So he says a moderate spike in glucose is okay unless one has metabolic derangement. Therefore, it is also important to note that the detriment of glucose applies to everyone. Some people can hold up to a greater beating than others. However, even if someone appears to tolerate something, it does not mean it is good for them. The body can compensate, tolerate, and defend itself from particular insults, but if that compensation is repeated over and over and over again the body will lose that ability to compensate and defend. The body can tolerate a windfall of glucose by spiking insulin (and leptin) to store what isn’t immediately burned for a rainy day (mostly as fat). But continuing to do this will wear the body out and will result in insulin and leptin resistance. Let’s look at some more science: There is no threshold for healthy blood glucose: Is there a glycemic threshold for mortality risk? Diabetes Care May 1999 vol. 22 no. 5 696-699 “…the lowest observed death rates were in the intervals centered on 5.5 mmol/l [99mg/dl] for fasting glucose and 5.0 mmol/l [90 mg/dl] for 2-h glucose. CONCLUSIONS: In the Paris Prospective Study, there were no clear thresholds for fasting or 2-h glucose concentrations above which mortality sharply increased; in the upper levels of the glucose distributions, the risk of death progressively increased with increasing fasting and 2-h glucose concentrations.” “Normal” blood glucose and coronary risk BMJ VOLUME 322 6 JANUARY 2001 “Khaw et al in this issue shows that glycosylated haemoglobin levels are positively associated with the risk of future coronary heart disease in a linear stepwise fashion, with no evidence of a threshold effect and independent of other common risk factors for coronary heart disease. These are the most convincing data available that the association between glucose and coronary heart disease occurs throughout the normal range of glucose.” Post-challenge blood glucose concentration and stroke mortality rates in non-diabetic men in London: 38-year follow-up of the original Whitehall prospective cohort study Diabetologia (2008) 51:1123–1126 “Results During follow-up of 18,406 non-diabetic men, 13,116 deaths occurred (1,189 by stroke). Plots of stroke mortality rates versus blood glucose identified an upward inflection in risk of death from stroke at about 4.6 mmol/l [82 mg/dl]. This upward inflection in risk could be adequately described using a single linear term above this threshold. Conclusions/interpretation; An incremental elevation in stroke mortality rates occurs with increasing post-challenge blood glucose.” 2010 WebMD How the Blood Sugar of Diabetes Affects the Body “At present, the diagnosis of diabetes or prediabetes is based on an arbitrary cut-off point for a normal blood sugar level.” ScienceDaily, Monash University (2008, August 22) Killer Carbs: Scientist Finds Key To Overeating As We Age published in ‘Nature’. “Dr Andrews found that appetite-suppressing cells are attacked by free radicals after eating and said the degeneration is more significant following meals rich in carbohydrates and sugars. ‘The more carbs and sugars you eat, the more your appetite-control cells are damaged, and potentially you consume more,’ Dr Andrews said.” Is There a Clear Threshold for Fasting Plasma Glucose That Differentiates Between Those With and Without Neuropathy and Chronic Kidney Disease? Am J Epidemiol 2009;169:1454–1462 “Recent studies suggest that no distinct glycemic threshold consistently differentiates individuals with or without retinopathy. The authors sought to determine whether the same was true [in a random sample of individuals] for other microvascular complications…Prevalence of peripheral neuropathy and chronic kidney disease gradually increased in relation to fasting plasma glucose, beginning at levels below the existing diagnostic threshold for diabetes mellitus of 7.0 mmol/L (126 mg/dL).” One-hour postload plasma glucose and risks of fatal coronary heart disease and stroke among nondiabetic men and women: the Chicago Heart Association Detection Project in Industry (CHA) Study. J Clin Epidemiol. 1997 Dec;50(12):1369-76 Stamler J. Northwestern University Medical School, Chicago, IL “Plasma glucose was determined one hour after a 50-gram oral glucose load… higher glucose was significantly associated with mortality from coronary heart disease, stroke, cardiovascular diseases, and all cause mortality in men and women. This large longitudinal study provides evidence that one-hour postload plasma glucose in the absence of clinical diabetes at baseline apparently is an independent risk factor for fatal coronary heart disease and stroke in middle-aged and older nondiabetic men and women, and also for cardiovascular diseases and for all cause mortality.” Glycated haemoglobin, diabetes, and mortality in men in Norfolk cohort of European Prospective Investigation of Cancer and Nutrition (EPIC°©Norfolk) BMJ VOLUME 322 6 JANUARY 2001 “HbA1c was continuously related to subsequent all cause, cardiovascular, and ischaemic heart disease mortality through the whole population distribution, with lowest rates in those with HbA1c concentrations below 5%. An increase of 1% in HbA1c was associated with a 28% (P < 0.002) increase in risk of death..." Glucose accelerates aging, oxidative stress… Pro-Aging Effects of Glucose Signaling through a G Protein-Coupled Glucose Receptor in Fission Yeast PLoS Genetics, March 2009 | Volume 5 | Issue 3 “…excess of glucose has been associated with several diseases, including diabetes and the less understood process of aging. On the contrary, limiting glucose (i.e., calorie restriction) slows aging and age-related diseases in most species…The pro-aging effect of glucose signaling on life span correlated with an increase in reactive oxygen species and a decrease in oxidative stress resistance and respiration rate. Likewise, the anti-aging effect of both calorie restriction and the Dgit3 mutation was accompanied by increased respiration and lower reactive oxygen species production.” Rather than being good for white blood cells, glucose can oxidize them… GLUCOSE CHALLENGE STIMULATES REACTIVE OXYGEN SPECIES (ROS) GENERATION BY LEUCOCYTES The Journal of Clinical Endocrinology & Metabolism, Vol. 85, No. 8, Aug. 2000 “Blood samples were drawn from 14 normal subjects prior to, at 1, 2 and 3 h following ingestion of 75 g glucose…We conclude that glucose intake…increases oxidative load [in leukocytes] and causes a fall in a-tocopherol concentration.” Sugar glycates. For those unaware, this is where glucose (and other sugars) combines with other essential molecules such as proteins and DNA affecting their shape and structure and preventing their proper function. This is a very bad. Glycation is one of the major molecular mechanisms that cause damage resulting in senescence that we notice as “aging”. That is why products of glycation, advanced glycated end products, are not coincidentally called AGEs. There is no threshold for glycation…more glucose, greater risk of glycation… Advanced glycated end products: a review Diabetologia (2001) 44: 129-146 “Glycation is concentration-dependent” Lipoprotein Lipase Mediates the Uptake of Glycated LDL in Fibroblasts, Endothelial Cells, and Macrophages. Diabetes 50: 1643–1653, 2001 “Protein glycation is a nonenzymatic reaction of glucose with susceptible amino groups that occurs at a rate linearly related to the plasma glucose concentration.” Significant amounts of highly reactive precursors to AGEs (advanced glycated end products) are formed after a single standard (with carbohydrate) meal… a-Dicarbonyls Increase in the Postprandial Period and Reflect the Degree of Hyperglycemia. Diabetes Care 24:726–732, 2001 “Chronic hyperglycemia is known to increase tissue glycation and diabetic complications, but controversy exists regarding the independent role of increased postprandial glucose excursions. To address this question, we have studied the effect of postprandial glycemic excursions (PPGEs) on levels of methylglyoxal (MG) and 3-deoxyglucosone (3-DG), two highly reactive precursors of advanced glycation end products (AGEs)….PPGE was determined after a standard test meal. Conclusion: Increased production of MG and 3-DG [AGEs] occur with greater PPGE, whereas HbA1c does not reflect these differences.” Insulin glycates contributing to insulin resistance…and its sequelae, diabetes, CV disease, obesity, cancer, and accelerated aging… Glycation of insulin results in reduced biological activity in mice. Acta Diabetol. 1997 Dec;34(4):265-70 “These data indicate that glycated insulin exhibits impaired biological activity which may contribute to glucose intolerance…” Glycation of LDL in non-diabetic people: Small dense LDL is preferentially glycated both in vivo and in vitro. Atherosclerosis. 2009 Jan;202(1):162-8 “CONCLUSION: Small-dense LDL is more susceptible to glycation and this may contribute to the atherogenicity of smalldense LDL, even in non-diabetic people.” Glucose directly contributes to aging and feeds cancer cells; Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression. FASEB, December 17, 2009 “Cancer cells metabolize glucose at elevated rates and have a higher sensitivity to glucose reduction…The altered gene expression was partly due to glucose restriction-induced DNA methylation changes…Collectively, these results provide new insights into the epigenetic mechanisms of a nutrient control strategy that may contribute to cancer therapy as well as antiaging approaches.” Raising glucose, raises insulin, increases insulin resistance… Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study. Diabetologia (2004) 47:31–39 “Conclusion/interpretation. When the plasma insulin response to oral glucose is related to the glycaemic stimulus and severity of insulin resistance, there is a progressive decline in beta-cell function that begins in “normal” glucose tolerant individuals.” High insulin leads to insulin resistance–what I’ve said for 2 decades Barbara B. Kahn and Jeffrey S. Flier, Harvard Medical School The Journal of Clinical Investigation, August 2000 | Volume 106 “Hyperinsulinemia per se can cause insulin resistance by downregulating insulin receptors and desensitizing postreceptor pathways, as was confirmed by overexpression of insulin in livers of otherwise normal transgenic mice. This transgene resulted in an age-related reduction in insulin receptor expression, glucose intolerance, and hyperlipidemia without any primary genetic defect in insulin action or secretion.” And again… Alternative Approach to Treating Diabetes Tested ScienceDaily (June 10, 2011) From; Deletion of Insulin-Degrading Enzyme Elicits Antipodal, Age-Dependent Effects on Glucose and Insulin Tolerance. Plos One June 2011 | Volume 6 | Issue 6 “It’s an example of too much of a good thing [insulin] becoming bad for you…chronic hyperinsulinemia seemed to actually cause diabetes. As they aged, the mice appeared to adapt to the chronically high insulin levels, for example, by reducing the number of receptors for insulin in their tissues. These adaptations make the mice less sensitive to insulin, which is the exact cause of type 2 diabetes.” And again… Insulin: In need of some restraint? Salk Institute Proceedings of the National Academy of Sciences,March 07, 2007 “the study reveals the “dark side” of high insulin production, the kind that results from over eating and obesity. “Insulin is very effective at lowering blood sugar, and promotes fat storage, preparing the animal for times when food may not be available,” he says. “But when the hormone [insulin] is produced at too high a level for too long, the body becomes insulin resistant and blood sugar and certain blood lipids gradually creep up, which can cause progressive damage to multiple organ.” I also know from treating hundreds of diabetic patients that reducing insulin and leptin via my diet that prevents insulin and leptin from spiking and keeps them low, rapidly improves insulin and leptin resistance, and greatly improves, if not altogether reverses, T2 diabetes and other chronic diseases of aging. The reduction in leptin and insulin happens first and appears to be a requisite. Others are now treating with a similar diet including Eric Westman and Mary Vernon who have published several papers. I could go on all day with studies such as this…and that’s mostly focusing on blood glucose (BG). But the main culprits in the chronic diseases of aging are hormones that glucose both powerfully affects and is affected by…such as insulin. Raising BG raises insulin

At det stort set er ligegyldigt hvordan du spiser passer ganske enkelt ikke, selv moderat indtag af sukker associeres med udvikling af hjerte-karsygdomme Omvendt er blodpropper og åreforkalkning totalt ukendte fænomener på sukker og fedtfattig vegansk kost. Der foreligger hård evidens for at vegansk kost giver 100% kontrol med disse sygdomme selv i svære tilfælde. Blodpropper og åreforkalkning er man således selv skyld i, for det noget man kan kontrollere 100% gennem kosten hvis man vil. Talsmænd for moderation og det hele er stort set ligegyldigt kan siges at bære en del af skylden for blodpropper og åreforkalkning. Low-carb diæter giver dig selvfølgelig bedst mulig blodglukose-kontrol og holder dermed bedst både diabetes og prædiabetes på afstand og udskyder disse sygdomme! I en forstand er vi alle metabolsk skadet, hvor prædiabetes er en lidt arbitrær fastsat grænse. Der findes ingen sikker tærskel for sikkert sukker-indtag, enhver afvigelse af blodsukker over baseline påføre kroppen skader, fx. gennem gradvis at forringe dit syn ved at beskadige cellerne. Det viser studier foretaget på raske mennesker. At mindske det glykæmisk load i kosten giver fin mening. Man kan også blive ramt af en bil eller så meget andet. Så det er i sidste instans et spørgsmål hvor du gider at gøre ud af det og hvor naturligt det ligger for dig. Man skal også leve.

Jeg kan ikke andet end at smile af dit indlæg. Jeg bliver qua min uddannelse og job undervist af fysioterapeuter. Vi diskuterede specifikt denne del af min OP " Tredje øvelse, skulder dislokationer ser vilde ud og dem er jeg betænkelig ved. Nogen kontra-indikationer? (alder, tidligere skader)." Dit bro-science du fra træningssalen besvarer ikke dette. Der sker nemlig med alderen typisk en række fysiologiske forandringer i skulderen, der gør at de fleste skal holde sig fra skulder dislokationer. Når du skriver "Erfaring + K.I.S.S. + "The principle of individuality"." forstår du desuden heller ikke at individuelle behov ændrer sig gennem livet, hvilket giver god mening at tage højde for, når vi snakker skuldermobilitet. Holdes den ikke vedlige, så lukker vinduet PERMANENT.

"Derudover så er statiske hold i virkeligheden ikke helt statiske. " Kan jeg godt følge dig i. Læste forresten en interessant artikel om at underarmens muskler (pronatorer og supinatorer) ofte er relativ svagere efter der er kørt bænkpres end tilfældet er med triceps. Kan måske være grund til at kigge på, om man skal træne underarme lidt mere (forudsat at man dermed ikke overtræner dem).

Godt billede TheCzech. Ingen tvivl om at man kan komme relativt hurtigt tilbage på kortere sigt. Jeg kunne dog godt tænke mig at se, fra folk der kommer længere ned i vægtklasse og har været det i måske +5 år. Jeg husker jeg som ung og tynd kæmpede for at få KG på arme. I dag er jeg ikke tynd, men mit indtryk er klart at bulerne på overarmerne kommer hurtigere igen (meget hurtigere end de vægte jeg er nået til nu berettiger til - hvis du forstår) Jeg trænede for et par uger siden for første gang tungere ben i mange år, hvor det blødte fra et utal af steder ned af benet når årer og kar sprænger. Konstant obs på ikke at få fibersprængninger/seneoverrivninger som den begrænsende faktor. Det bedste IMO er klart at ride på 'bølgen' fra man er ung og så aldrig falde af. Det synes utrolig kompliceret at komme igen senere i livet. Fra 40 års alderen mistes desuden specifikke muskelopbyggende hormoner.

Se nedenfor.

Der gives en populær fremstilling af et kompliceret emne, så alle skulle kunne forstå hvad det drejer sig om . Dernæst skriver jeg, "Så kom gerne med indspark og artikler " Dit indlæg giver i den sammenhæng slet ingen mening. Nu har jeg skimmet dine indlæg og du har et generelt problem, som jeg ikke gider tid på at forklare her.

Skru op for dit generelle indtag lyder som god ide. Du kan også dagligt begynde at spise Avocado og (val)nødder. Skal ikke nødvendigvis så meget til for at vende regnskabet.

Det kniber vist med at huske. En person spurgte efter et underkropsprogram uden dødløft og squat, fordi han var svækket. Nogen bragte alligevel squat (+varianter) på banen, hvor jeg bragte jeg hip-thrusts på banen. Med hip-thrusts ligger man ned uden det balancemoment som gør de andre underkropsøvelser anstrengende. Fysioterapeauter bruger ofte Glute-bridges (lidt henad hipthrusts) som første underkropsøvelse til folk der er svækkede. Jeg kender godt min besøgstid, og hvornår lige den øvelse skal/kan doseres. F.eks. banker jeg afsted på Hip nu for at gaine masse, mens jeg efter længere pause forbereder mine knæ (sener) til benpres. Giver perfekt mening. Jeg udnytter tiden og den masse skal ikke gaines senere. Intelligent træning. Og trådstarteren her (hende har du måske glemt i alt det andet?) kan se ud til at have et problem/skuffelse over ikke at føle squat i bagdelen som forventet. Så er det naturligt at sige hun måske ikke går dybt nok i squat eller bør kigge sig om efter hip-thrusts og benpres (sidstnævnte vælger man selv hvilket område man fortrinsvis vil stimulere). Jeg har siden sidst set flere kvinder der bruger smedestativet til hip-thrusts, med ekstremt gode resultater. Kvinder er interesseret i resultater, mens mange styrkeløftere ikke kan tænke sig fri af (squat kulturen og "de tre") omkring deres egen sport. Jeg mener at alle af sundhedsmæssige årsager og hver dag burde squatte med ingen eller lettere vægt (for kropskordination, knæ, fordøjelse også videre). Jeg har derimod aldrig anbefalet benpres kombineret med hip-thrusts til alle. Jeg kan ikke se hvad fleste styrkeløftere skal bruge benpres til. Benpres er klart bedre til at køre mange reps 12-25 uden lockout så man får bentræning med lang TUT, der stimulere vækst i især type 1 fibrene - som præcis gør at bodybuildere/nogle banecykelryttere har større muskler end vægtløftere og styrkeløftere!. Med squat der stiller større krav til stabilitet kan det være svært at holde op-spændet under lang TUT. Derfor køres squat ofte med lavere repetitioner og med lockout mellem hver rep (der tager intensitet ud af øvelsen/forlårene). Giver perfekt mening. Der blev desuden for nylig postet en video af en cykelrytter med meget store lår der ligger et helt niveau over de andre styrkeløftere i samme squat konkurrence. Cykelrytteren benpresser (også) med mange reps. Giver perfekt mening. De færreste der vil udvikle deres forlår kan nøjes med squat - men laver noget ekstra. Folk afslører jo sig selv. I de perioder hvor jeg kørte tung benpres (evt. negativer) - var der TOTALT UDSOLGT i forlårene bagefter - uden noget behov for at køre leg-extension eller andet gøgl. Jeg er sikker på at jeg udviklede mit (krudtfrie) genetiske potentiale efter 9 års træning. Jeg blev spurgt af flere interesserede atleter fra et førende ishockey-hold om hvordan jeg havde trænet for at opnå mine resultater.

Se nedenfor

Jeg synes i reglen at Troels (modsat mange andre herinde) skriver interessante indlæg og kommer med gode bud. Men jeg synes tunge statiske holds er spekulativt når vi taler principper for hypertrofi, navnligt fordi der ikke sker bevægelse (og dermed mikrooverivning) af underarmens muskler. Hammer-curls (Troels vist nævner) med twist hjalp stort på mig selv, men jeg mener der skal mere forskelligartet bevægelse til for at udvikle alle underarmens muskler. Jeg var selv fra de tidlige teenageår fascineret af de mange muskler i underarmen der er i spil på min far som er smed. Mænd og kvinder der dødløfter relativt tungt har langtfra alle god underarmsudvikling. Når jeg ser på min fars arbejdsplads, så har samtlige kvinder og mænd veludviklede underarme. Jeg vil ikke være bange for at lave øvelserne med håndvægt i forhold til håndled. Jeg har prøvet at hjælpe til på min fars arbejde (speciel slags smed) og håndtere værktøjerne (der ofte er tunge i den lange ende) og de tunge metalplader (man ofte holder i kanten af) og det er ekstremt hårdt for underame selvom man er vant til tunge dips, pullups, hammer-curls, dødløft. Det var til stor sjov for min far og kollegaer. Så mit råd er at du bare skal køre underarmsøvelserne roligt, så bør der ikke opstå problemer med led. Heller ikke rotation med håndvægte. Stille og roligt. Ulnar deviation (måtte slå den op) har jeg svært ved at se kommer i spil under normal styrketræning. Det kunne tænkes at den kunne yde ekstra beskyttelse/give stabilitet til albuen (i tunge triceps øvelse). Men det er ren spekulation.

KStar kan jeg genkende nu. Jeg har tidligere set en længere interessant video med ham, hvor han analyserede forskellige menneskers holdning og måde at bevæge sig på, og spottede led der fungerede som "hængsler", der på sigt kan udvikle slidgigt og andet skidt. Var ikke klar over han var så produktiv med videoer. Der er noget at kigge på hvad angår skuldre (og andet). Man kan også intuitivt bevæge, lege og strække sig til meget selv. Man "må" det meste. Alligevel behøver man viden om de stræk, hvor man kan lave irreversible skader på f.eks. tynde ledkapsel(er). Det er surt at opdage bagefter.

Kommentar til VenaN's indlæg Jeg har tidligere talt om ikke at sammenligne iso med basis hvad angår EMG. EMG er et fingerpeg, så kommer der en række andre faktorer man bør kigge på. Jeg mener også det er på tide at bruge MRI scanninger der fokuserer på resultatet af øvelser, så kan der ryddes op i øvelser. EMG er dog yderst relevant. Den gjorde jeg fik øje på donkey calf-raises der giver større udslag på læggen end samtlige andre lægøvelser OG samtidig ved vi at i donkey calf-raises har langt større træk på læg (som den KAMP-isolerer). ALLIGEVEL synes folks foretrukne lægøvelser at være stående læg, siddende i maskiner eller andet, hvilket er idiotisk. Når man har aflæst EMG, går man videre og sammenligner øvelsernes andre kvaliteter (stræk, intensitet). Barbell Rows scorer også højt i forhold til mange øvelser. Jeg har lige set klip med Payam der laver den, vægten nærmest droppes det første stykke på den excentriske (karakteristisk for selve øvelsen), hvilket koster intensitet i den afgørende hypertrofi-skabende negativ. Derfor vil jeg personligt, vælge andre rygøvelser.

Jeg lavede selv en Nordic Raise med mellemrum til knæene så knæene gik fri. Både bedre for knæ og øvelsen bliver imo mere effektiv da man bliver mere stabil .

Gav lidt for hurtigt Niels ret i denne, "Et dip bælte og 2 kasser er ligeså gode" Nogen bliver med hip-belt squat fra kasser tvunget til at squatte i bredere stand, end de normalt gør. Det løser platformen. Men til den pris kunne man nok hekse noget selv, eller få andre til det.