A Sugar Substitute That’s Good For You? The Science Behind Allulose - with Dr. Bikman
Allulose appears to be one of the more metabolically neutral sweeteners studied so far — although reducing total sweetener intake may matter more than swapping types
Dr. Benjamin Bikman with Dr. David Perlmutter
Episode aired Dec 4, 2023·Page synthesised Mar 26, 2026·Last reviewed Mar 26, 2026
What this episode covers
- Benjamin Bikman, a Brigham Young University metabolic researcher, explains the mechanistic case for allulose — a rare sugar that does not appear to spike insulin and may activate GLP-1 and AMPK pathways.
- Replacing fructose with allulose may reduce uric acid production in mechanistic models, with potential downstream effects on insulin sensitivity, fat oxidation, and possibly brain ketone availability.
- The episode is mechanism-rich and the substitution argument is biologically plausible; large clinical-outcome trials remain limited, so the practical framing is sweetener-of-choice for people who already use sweeteners, not a stand-alone metabolic intervention.
Why it matters
Bikman argues that allulose, a rare sugar that does not raise insulin and may activate GLP-1 and AMPK pathways, is a metabolically favorable alternative to fructose for people managing insulin resistance. Mainstream metabolic research broadly agrees that high fructose intake contributes to insulin resistance, fatty liver, and uric acid elevation, and that GLP-1 activation is a well-validated metabolic target (it is the mechanism behind semaglutide). What is contested is whether allulose at typical home-use doses produces clinically meaningful effects on insulin sensitivity, body weight, or long-term outcomes — human trials remain small and short-term. What survives the disagreement is the foundational move: reducing total added fructose intake (especially from sugar-sweetened beverages and ultra-processed foods) carries the strongest evidence; sweetener substitution sits one layer below that.
What stands out
- Allulose may activate GLP-1 — the same pathway as semaglutide-class drugs — without raising insulin, although the magnitude of the human effect is much smaller than pharmaceutical GLP-1 agonists and is still being established at typical home-use doses.
- Replacing fructose with allulose may reduce uric acid production in mechanistic models; this is one of the more specific and biologically plausible claims in the episode, although direct outcome data in humans remain limited.
- Like several low-calorie sweeteners, larger doses of allulose may cause bloating or diarrhea in some people because of incomplete absorption — individual tolerance varies and matters for daily use.
Best-supported action
The single highest-leverage move from this episode, anchored in the strongest evidence the speaker presents.
Reduce added fructose first — especially liquid calories like sugar-sweetened beverages and fruit juice. Sweetener substitution matters less than the total reduction.
Where to start
Small low-friction starters covering the main moves from this episode.
- Audit your daily added-sugar sources (drinks, sauces, snacks) and pick one to remove or reduce this week
- If you use sweeteners in coffee or cooking, try allulose as a substitute and note how appetite and cravings respond over 2-3 weeks
- Ask your next routine bloodwork to include fasting insulin alongside fasting glucose
Other supported actions
Further actions discussed in this episode, ordered from strongest to weakest evidence. This is one expert's view, the full topic compares and ranks across experts.
- Reduce added fructose at the source — particularly sugar-sweetened beverages, fruit juices, and ultra-processed foods that list high-fructose corn syrup, agave syrup, or large amounts of added sugar. This is the move with the strongest evidence base and the lowest downside.Moderate evidence
- If you continue to use sweeteners, allulose appears to be one of the more metabolically neutral options based on early human and mechanistic data. It may be used as a substitute for sugar in many beverages and recipes, although it browns differently and is roughly 70% as sweet as sugar, so quantities and behavior in baking can differ. Long-term safety data are limited, so this is a sweetener-of-choice positioning rather than a recommended daily intake.Moderate evidence
- Ask your doctor to add a fasting insulin test to your next routine bloodwork. Elevated fasting insulin can sometimes flag insulin resistance years before fasting glucose shifts, although fasting insulin is not yet universally included in routine screening guidelines — which is why you may need to specifically ask for it. The result can change the conversation about prevention timing.Strong evidence
Full context, impact ratings, and timing — available in related topics
Questions to take to your doctor
- Given my recent blood glucose results, would adding fasting insulin to my next bloodwork meaningfully change how we think about my metabolic health?
- Given my current uric acid level (or gout history, if relevant), would reducing fructose intake from drinks and processed foods be a useful first step, and do you have a specific intake target in mind?
- Given my current medications and conditions, is regular allulose use likely to be safe, particularly if I have a history of digestive sensitivity?
- Given my family history (diabetes, fatty liver, cardiovascular), at what fasting insulin range would you consider it worth acting on, even if my fasting glucose is still normal?
- If I am working toward weight loss or appetite regulation, would you consider allulose a useful adjunct, or are there foundational levers (sleep, activity, food quality) that should come first in my case?
Full doctor prep with ranked questions available in the full topic page
Context
BYU metabolic researcher who frames insulin resistance as the connector across multiple cardiometabolic conditions. The insulin-resistance-as-cardiovascular-driver framing is broadly mainstream; the carbohydrate-insulin model as the primary driver of obesity is still actively contested in the energy-balance literature. Bikman has commercial exposure (co-founder of HLTH Code and Insulin IQ, author of Why We Get Sick), which is relevant context when he is the source of a specific protocol or substance recommendation, although it does not itself invalidate the underlying physiology he discusses. Strongest on mechanism; worth pairing with conventional clinical-outcome evidence when the conversation moves from mechanism to recommended daily protocol.
This episode does not prove that allulose directly prevents Alzheimer's disease, reverses fatty liver, or replaces medical treatment for type 2 diabetes. The case Bikman makes is largely mechanistic — well-described biology around GLP-1, AMPK, insulin signaling, and fructose-uric-acid metabolism — with supportive evidence drawn from small human studies and animal data. Large randomized trials on clinical outcomes are limited. Practical downsides also exist: like several low-calorie sweeteners, larger doses of allulose may cause bloating or diarrhea in some people because of incomplete absorption, which limits how much most people will tolerate in a day.
The link from allulose to brain health is extrapolated. Bikman's lab has shown that brains affected by Alzheimer's preserve the ability to use ketones, and allulose does not appear to disrupt ketosis. The logical chain (allulose → no insulin spike → preserved ketosis → ketones available for the brain) is biologically plausible but not the same as direct evidence that allulose meaningfully changes Alzheimer's risk in humans.
Both experts have commercial exposure in the metabolic-health space (Bikman with HLTH Code and Insulin IQ; Perlmutter with his own brand), which is relevant context but does not itself invalidate the science discussed. Bottom line: allulose has a plausible mechanistic profile and is a defensible sweetener-of-choice if you already use sweeteners — but the foundational metabolic move is still to reduce total added fructose, particularly from liquid calories, and that lever sits one rung above any substitution strategy.
Where people go wrong
- Assuming fasting blood glucose alone tells you whether your metabolic health is on track.Insulin resistance can develop years before fasting glucose shifts. By the time glucose is elevated enough to flag prediabetes, the underlying metabolic dysfunction may have been progressing for some time.
- Assuming uric acid concerns come mainly from red meat or alcohol.Fructose metabolism is one of the more consistently documented dietary drivers of uric acid production. People who reduce meat but keep high-fructose intake (juice, sweetened drinks, fruit-heavy diets) may miss the larger lever.
What to expect over time
- First 1-2 weeksIf you reduce added fructose (especially from drinks) as the primary move, you may notice steadier between-meal energy and reduced sweet-craving intensity within days. If you also switch to allulose where you previously used sugar, evening cravings sometimes settle as the GLP-1 signal kicks in. Watch for mild gastrointestinal effects at higher allulose doses — some people tolerate it better than others.
- Weeks 3-8Eating patterns often stabilize as the lower-fructose baseline sticks. Appetite tends to be calmer between meals. If you have access to repeat bloodwork, fasting insulin can sometimes start trending lower at this point, although individual variation is substantial and meaningful change usually requires more time.
- Months 2-6+If the change holds, this is the window where fasting insulin and uric acid may show measurable improvement on bloodwork. The size of the change depends heavily on starting point, total caloric and carbohydrate context, sleep, activity, and other foundational levers. Allulose substitution is one input among many, not a stand-alone driver.