#9 CGMs, Blood Flow, Low Carb and Muscle

Time to Roll Our Sleeves Up.

With the rise in popularity of continuous glucose monitors (CGMs), I wanted to take a look at the pros and cons in this issue. And, yes, there are cons. Then we’ll look at the latest meta-analysis of low-carb diet interventions that you might have heard about and see what all the hype has been about. Do low carb diets have a substantial edge after all and should you consider trying (or sticking with) one? After that, did you know that insulin resistance can seriously affect how blood flows through your tissues and organs, subtly starving organs of nutrients and oxygen? This can have very unpleasant health effects and it’s worth your time to understand it and how you can fix the issue. And, finally, we end with how to build healthier, hungrier muscles that are ready and willing to soak up all that blood glucose that’s been wreaking havoc (not to mention, giving you huge reserves of strength and function that will last you well into older age).

So, without further ado, let’s jump in.

CGMs and ‘Time‑in‑Range’ in the Real World

Continuous glucose monitors (CGMs) are all the rage right now, and feel like a window into your metabolism - but the picture it gives you needs interpreting. It is not reading your blood glucose directly, the way a finger-stick monitor does; it’s reading glucose concentration in the fluid around your cells, the interstitial fluid. As glucose takes some time to diffuse from your blood into this interstitial fluid, a CGM reading always lags behind the bloodstream. In slowly changing conditions between meals or overnight, this is no problem. But, when glucose is rising or falling quickly the delay can be around 10 - 20 minutes. This can give a false sense of security when you check it soon after a meal, or a feeling that your after-eating exercise isn’t working to bring your blood sugar down as quickly as you might like.

Continuous monitoring gives us a new, number to track: time-in-Range (TIR). This is simply the percentage of time you spend in whatever target you (or your doctor) choose. The two ranges you see quoted commonly, and the consequences of staying within them, are as follows:

• Standard clinical target (used in virtually all type-2 trials and ADA/EASD guidelines): 3.9–10.0 mmol/L (70–180 mg/dL) → Each 10% increase in TIR in this range is associated with roughly a 0.4–0.6% drop in HbA1c and, more importantly, a measurable reduction in progression of retinopathy, nephropathy, and cardiovascular events (Beck et al., Diabetes Care 2019; Lu et al., Diabetes Care 2020).

• “Physiological” or non-diabetic mimicking target: 3.9–7.8 mmol/L (70–140 mg/dL) → In people without diabetes this is roughly where glucose lives >90–95% of the day. In reversal-focused patients, pushing TIR in this tighter band to >80–85% correlates with actual remission-level HbA1c <6.0% without meds (Taylor et al., Diabetologia 2021; Hall et al., 2023 personal communication from the ReTUNE cohort).

Crucially, TiR has now been shown to be an independent predictor of complications, separate from HbA1c. Studies from Beck and colleagues (Beck, Diabetes Care, 2019) and others have found that higher TiR is associated with lower rates of retinopathy, kidney disease and nerve damage even at the same HbA1c. Every extra 10% of time spent in range seems to matter. But the goal is not perfection; it is to slowly nudge the pattern in the right direction.

And, always remember: what matters most is not any single spike or dip, but the pattern across weeks. Are you inching towards more time in range? Are the post‑meal peaks softening? Is the graph getting a little quieter? That’s progress - one step at a time.

But there is an emerging problem CGMs are causing: they can subtly create a kind of carb‑phobia or push you towards food anxiety and obsession with details where it is not warranted. It’s easy to start watching every little rise after a meal and panic. Sometimes that’s fair - if breakfast is a pint of orange juice, cereal and toast, the CGM will spike and you should learn something useful from that. But more often it’s a perfectly normal, moderate meal creating a rise that looks dramatic on the screen, and people immediately try to “fix” the number by cutting carbs or overall eating to the bone.

This is where the tool becomes the trap.

A glucose rise is always a mixture of the food and your current metabolic response to it. Reducing carbs will flatten the spike, but that treats the symptom, not the insulin resistance that caused the exaggerated response. Managing symptoms is fine, and sometimes necessary, but it is not the main job.

You can reduce spikes without doing something more drastic, and that may be more sustainable and sensible in the longterm. Lowering total energy intake, increasing fibre, cutting back on ultra‑processed foods, walking after meals, improving sleep, and gradually clearing visceral and liver fat will all soften the response to carbs/meals. As these underlying systems improve, the same food that once sent you to 11 mmol/L might later peak at 7, and eventually 6, without removing it from your life.

You can run harmless experiments while you work on those deeper levers. A 2015 Diabetes Care study (Shukla, Diabetes Care, 2015) showed that eating protein and vegetables before the starch component of a meal reduced the 60‑minute glucose rise by about 37%, simply by slowing gastric emptying and smoothing absorption. This does not fix insulin resistance, but it can take the edge off a difficult meal.

And if your CGM shows a gentle rise between 4 a.m. and 8 a.m., that is usually just the dawn phenomenon - a normal surge of hormones telling the liver to release stored glucose as part of your normal “wake-up program”.

So don’t let the CGM bully you into accidental carnivore, any kind of food paranoia, or cause you to lose sleep. The goal is not to flatten the graph entirely - a mixed blood glucose landscape is completely normal physiology. So, unless you see something very worrying, think of a CGM as a way to watch your blood glucose change over several weeks/months, and fix the underlying disease process rather than the scary symptom of it.

Insulin, Nitric Oxide, and Why Blood Flow Matters

Here is something not widely enough discussed: insulin resistance disturbs normal blood flow through tissues and organs and can lead to fatigue, discomfort and, ultimately, serious diabetic complications.

Insulin does not just help your cells absorb glucose, but also helps deliver nutrients and oxygen to your tissues (and clear away waste products) by changing local blood flow. Your blood vessels have a one-cell thick layer made of specialised cells called endothelial cells, and the whole lining is called your endothelium. When insulin levels increase after a meal, it is absorbed by your endothelium and activates an enzyme called endothelial nitric oxide synthase (eNOS), which produces nitric oxide (NO). NO spreads into the lining of your blood vessels and relaxes the muscles that keep them tight. These small vessels that feed your muscle and other organs then open up and blood flow increases, bathing your cells in the nutrients they need and taking away wastes. But …

In insulin resistance, that signal loses its potency. The branch of the insulin pathway responsible for NO production is selectively impaired, while other, “constrictor pathways” keep on working as normal. Several modern studies have shown this clearly. Zhang and colleagues (Zhang, Am J Physiol, 2011) demonstrated that people with insulin resistance have a markedly blunted ability to recruit their muscle microvasculature (small blood vessels) in response to insulin, even when total limb blood flow looks normal. Alekseyeva’s group (Alekseyeva, Curr Hypertens Rep, 2020) found that the vasodilator (blood vessel widening) arm of insulin signalling is weakened in metabolic syndrome, while the vasoconstrictor (blood vessel narrowing) arm is preserved. And, this is more than just a nuisance: cells that are chronically deprived begin to malfunction, often sending out little “help!” signals in the form of inflammatory mediators - chemical signals that influence the local tissues and wider body.

In terms of blood glucose, this means fewer capillaries open after meals, less glucose and insulin reach the muscle, and the pancreas has to pump out more insulin to compensate. Post‑meal glucose rises higher and stays higher. Many people with early type‑2 diabetes describe post‑meal heaviness, thick legs, or that dreadful wave of fatigue. And, unfortunately, along with the discomfort, comes a secondary issue - the increased insulin exposure only increases the insulin resistance in your endothelium for the next meal.

And it is not just your muscles that suffer. Your brain, kidneys, heart, nerves and eyes all depend on tiny blood vessels opening and closing correctly. When NO signalling fails, you are not just looking at high glucose but system‑wide under‑perfusion. Retinal vessels in your eyes that cannot dilate properly are more vulnerable to damage. Kidney filtration units struggle when the blood vessel tightness is chronically high. Small vessels in your heart stiffen and stop responding. Nerves lose some of their oxygen and nutrient supply. This is one reason complications like retinopathy, nephropathy, neuropathy and cardiovascular disease cluster the way they do.

The hopeful part is that this blood flow problem is highly responsive to the very same levers we use for diabetes reversal.

Muscle contraction activates a separate NO‑producing mechanism that does not rely on insulin. We know that breaking up sedentary time and walking after meals improves glucose control; part of that effect is likely through improved microvascular function.

Strength training is another very powerful intervention. Ballard’s 2022 trial (Ballard, Med Sci Sports Exerc, 2022) showed that eight weeks of resistance training increased eNOS content, improved flow‑mediated dilation (a measure of ability of your blood vessels to open up) and reduced post‑meal glucose spikes in people with insulin resistance. In parallel, weight loss trials such as those reported by Lee’s group (Lee, J Clin Endocrinol Metab, 2019) have shown that reducing visceral and liver fat restores eNOS function and NO availability, independent of changes in fitness.

So, given its importance, what else can we do to target this problem beyond the usual weight-loss and exercise? There are good reasons to believe that a few dietary factors can nudge things in the right direction. These are not magic fixes and they cannot substitute for movement, sleep or weight loss, but they can gently support endothelial function. Don’t discount this because small nudge compounds over time to a larger effect - and this is especially the case for slimmer diabetics, who are working with smaller margins.

Dietary nitrates from beetroot and leafy greens make NO through a pathway that bypasses impaired eNOS. Several trials have shown improved flow‑mediated dilation and blood perfusion in insulin‑resistant adults (Kapil, Hypertension, 2015; Lara, J Appl Physiol, 2016). The result is that nitrates can lower blood pressure and boost athletic performance, and they may have benefits for cardiovascular disease. This pathway is the same one that is targeted by ED drugs like viagra and tadalafil. The dose where effects become noticeable is around 400 mg/day, and this can be reached by a mix of dark green leafy vegetables and a few deliberate boosts from high nitrate foods (beetroot, rocket/arugula, celery, lettuce, kale, etc.). See this paper for more detail on the science and food lists: paper.

Polyphenols, especially from cocoa flavanols (a type of polyphenol), berries and olives, and non-starchy vegetables help by protecting NO from breakdown and by modestly increasing eNOS activity. Cocoa flavanols have been shown to improve endothelial function within hours, with parallel gains in insulin sensitivity (Grassi, AJCN, 2008; Schroeter, PNAS, 2006) - a good reason to include cocoa & cacao in your diet. (NB: the powders are much higher in polyphenol content than even the best dark chocolate).

L‑citrulline, a precursor to arginine, is used by your body needs to produce NO. It avoids the first‑pass breakdown that undermines arginine supplements, which you might have heard of. Trials show small but meaningful improvements in blood vessel stiffness and NO bioavailability (Ochiai, Circulation, 2012).

And potassium‑rich whole foods (think vegetables, dairy, potatoes, pulses) improve blood vessel smooth‑muscle relaxation and lower blood pressure, partly by supporting NO signalling. Low potassium intake is consistently linked to reduced NO and higher vascular tone (blood vessel tightness). Beyond metabolic health, correcting a low potassium intake - which is very common - has fairly large effects on high blood pressure and heart health. As well as food sources, consider using a salt substitute like LoSalt that replace some of the sodium with potassium - but speak to your doctor first if you are on any medications that affect how your body handles potassium.

So, it’s a good idea to think how you can work some of these in to your baseline diet daily to reap the benefits while you focus on diabetes reversal more broadly. And, it is worth getting these from real food sources, not pills and powders.